Abstract
Background
Pressure ulcers are a largely preventable complication and an important patient-safety concern in community and home-care settings. Evidence from primary care–led home-care cohorts remains limited, particularly regarding how routine functional and laboratory markers relate to pressure ulcer presence. We examined associations between mobility, nutritional indicators, feeding route, and inflammatory markers—including serum albumin and the C-reactive protein (CRP)–to–albumin ratio (CAR)—and pressure ulcer presence in adults receiving home-care services.
Methods
This retrospective, cross-sectional study was conducted in a primary care–led home-care unit. Records of 983 patients screened between October 1, 2024 and January 14, 2025 were reviewed. Adults with limited mobility (semi-mobile or immobile) who had same-day albumin and CRP measurements and a documented Norton assessment were included. Pressure ulcer presence served as the primary variable of interest. CAR was calculated using same-day CRP and albumin values. Group comparisons, ROC analyses, and multivariable logistic regression were performed; calibration was assessed using the Hosmer–Lemeshow test. A complete-case approach was used.
Results
The analytic cohort included 328 patients (mean age 77.8 ± 15.0 years; 68.6% female). Pressure ulcer prevalence was 8.2% (27/328). Ulcer prevalence was higher in immobile than in semi-mobile patients (16.4% vs. 4.1%; p < 0.001) and differed by feeding route (p < 0.001). Patients with ulcers had lower albumin (35.8 ± 4.1 vs. 38.0 ± 4.5 g/L; p = 0.015) and lower Norton scores (12.3 ± 2.5 vs. 14.6 ± 2.6; p < 0.001). CAR was higher in the ulcer group (0.421 [IQR 0.61] vs. 0.157 [IQR 0.38]; p = 0.005) and showed modest discrimination (AUC 0.662; 95% CI 0.559–0.765). In multivariable analysis, oral feeding (vs. non-oral) was associated with lower odds of ulcers (OR 0.116; 95% CI 0.028–0.481; p = 0.003) and semi-mobility (vs. immobility) with lower odds (OR 0.291; 95% CI 0.121–0.700; p = 0.006); albumin showed a non-significant trend (p = 0.069). The combined model yielded an AUC of 0.760 (95% CI 0.663–0.857) with adequate calibration (Hosmer–Lemeshow p = 0.335).
Conclusions
In primary care–led home-care patients with limited mobility, pressure ulcer presence was associated with functional dependency (mobility and feeding route) and higher inflammatory burden. CAR may provide complementary information alongside functional assessment, but findings are exploratory and require external validation. These findings may inform population-level prioritization of preventive care in community and home-care services, rather than individual clinical decision.
Keywords: Pressure ulcer, Home care services, Immobility, Enteral nutrition, Serum albumin, C-reactive protein, Risk assessment
Introduction
Pressure ulcers (PUs) represent a common public health problem worldwide, with reported prevalence rates reaching up to 72.5% across different clinical and geographic settings [1]. They constitute a frequent complication to which many patients are vulnerable. Pressure ulcers are painful, economically costly, and adversely affect the quality of life of both patients and their caregivers; importantly, they are largely preventable [2]. In community and home-care settings, pressure ulcers are increasingly viewed as a patient-safety and care-quality issue that requires proactive risk identification and coordinated prevention within primary care–led services rather than episodic, wound-focused responses [3, 4]. Nutritional insufficiency and inadequate dietary intake are among the key risk factors for the development of pressure ulcers and for impaired wound healing. Unintentional weight loss and malnutrition are major contributors to pressure ulcer development [5].
Reduced mobility, sensory impairment, and inadequate nutrition are the principal factors that markedly increase the likelihood of pressure ulcer formation [6]. Nutritional status plays a central role in wound healing, and evidence suggests that nutritional support provided to individuals at risk can reduce the incidence of pressure ulcers by approximately one quarter [7]. Poor nutritional status is therefore considered a fundamental risk factor for pressure ulcer development. Moreover, insufficient food intake has been shown to be associated with both the occurrence of pressure ulcers and prolonged healing time [8]. Primary care and home-care teams are uniquely positioned to operationalize these risk factors, as mobility, feeding dependency, and basic laboratory tests are routinely available during longitudinal follow-up and can support pragmatic risk stratification [9].
Careful assessment of factors central to the pathophysiology of pressure ulcers—including sensory loss, malnutrition, inactivity, immobility, and reduced tissue perfusion—is critical for planning effective prevention strategies and organizing appropriate care. In this context, guidelines developed by the National Institute for Health and Care Excellence (NICE) and the joint recommendations of the European Pressure Ulcer Advisory Panel (EPUAP), the National Pressure Injury Advisory Panel (NPIAP), and the Pan Pacific Pressure Injury Alliance (PPPIA) emphasize the importance of comprehensive clinical evaluation targeting these risk factors [10]. However, translating guideline recommendations into day-to-day primary care–led home-care workflows remains challenging, and real-world evidence that uses routinely collected home-care variables to inform prevention priorities is still comparatively limited [3, 9].
In individuals with pressure ulcers, resting energy expenditure may increase while energy intake remains insufficient [11]. Standard clinical approaches used to estimate energy requirements may underestimate true metabolic needs in this population. Accordingly, daily energy intake (kcal/kg/day) should be adjusted upward to meet actual energy demand, and nutritional support should be provided when malnutrition is present [12]. Malnutrition is associated with adverse clinical outcomes, including an increased risk of mortality; therefore, early identification of existing or potential nutritional deficits enables timely intervention to limit further deterioration in nutritional status [13]. From a primary care perspective, the most actionable question is often not the precise caloric prescription, but which easily measurable indicators should trigger intensified preventive bundles—such as repositioning support, caregiver education, pressure-relieving equipment, and nutritional assessment—during home visits [3, 9].
Nutritional support may facilitate wound healing; however, evidence regarding specific interventions remains inconsistent. In patients who are malnourished or at risk of malnutrition, a daily protein intake of 1.25–1.5 g/kg and an energy intake of 30–35 kcal/kg are recommended, with adequate hydration encouraged when consistent with care goals and clinical condition. Supplementation with micronutrients such as zinc, arginine, and vitamin C may be beneficial, although evidence of benefit in patients without nutritional deficiency is inconclusive [10]. Accordingly, observational studies in primary care–linked home-care cohorts can add value by clarifying how routine markers of nutritional reserve and dependency cluster with pressure ulcer presence in real-world practice [9].
Enteral nutrition refers to the provision of nutrients via the gastrointestinal tract, either orally or through feeding tubes, including specialized diets or supplements in addition to normal intake. Parenteral nutrition involves the administration of nutrients directly into the bloodstream via intravenous infusion or intramuscular injection. Whether the route of nutritional delivery (i.e., oral feeding, tube feeding, or parenteral nutrition) plays a definitive role in the prevention or treatment of pressure ulcers remains unclear, and there is currently no conclusive evidence that nutritional interventions alone confer a clear benefit in this context. Further high-quality research is therefore required [14]. In community-acquired pressure ulcers, risk profiles may differ from those observed in inpatient settings, and mixed evidence underscores the need for setting-specific risk characterization to guide prevention in community and home-care environments [3].
Systemic inflammation may interact with nutritional status and frailty. Composite indices such as the C-reactive protein–to–albumin ratio (CAR) have been investigated as markers of frailty and adverse outcomes in hospitalized older populations [15]. However, the role of inflammation–nutrition composite biomarkers in pressure ulcer risk assessment—particularly in non-hospitalized settings—has not been fully elucidated. Because both CRP and albumin are widely available in routine care, composite inflammation–nutrition markers may offer a pragmatic adjunct to functional assessment in primary care–led home-care, provided their performance is interpreted cautiously and externally validated [3].
From a public health and health-services perspective, pressure ulcers represent a largely preventable source of morbidity, care burden, and avoidable healthcare expenditure. As populations age and home-based care expands globally, particularly in low- and middle-income settings, identifying low-cost, routinely available indicators that can support prioritization of preventive care has become increasingly relevant.
Unlike inpatient settings, community and home-care services often operate with limited resources, emphasizing the need for pragmatic risk signals that can inform visit frequency, caregiver support, and allocation of preventive equipment rather than individualized therapeutic decision-making.
Therefore, the aim of this study was to evaluate the associations between mobility status, nutritional indicators, feeding route, and inflammatory markers—including serum albumin and the CRP/albumin ratio—with the presence of pressure ulcers in a cohort of adult patients receiving home-care services.
Materials and methods
Study design and participants
This retrospective, cross-sectional observational study was conducted among adults registered in a primary care–led home-care unit. During the study period (October 1, 2024 to January 14, 2025), the medical records of 983 patients were screened. Inclusion required limited mobility (semi-mobile or immobile), availability of serum albumin and C-reactive protein (CRP) results recorded on the same calendar date in the laboratory records (date-level “same-day” matching), and a documented Norton pressure ulcer risk assessment at the evaluation time-point. Patients were excluded if they were fully mobile, if albumin and/or CRP were not available with same-day date matching, if the Norton assessment was not documented at the evaluation time-point, or if key variables required for the planned analyses were missing. The final analytic cohort consisted of 328 patients.
Variables
The first aspect we examined was the presence of pressure ulcer (yes/no) at the evaluation time-point, as documented in the routine skin/wound assessment record in the home-care file. The available records did not allow reliable determination of ulcer onset (incident versus pre-existing); therefore, the outcome reflects presence at assessment rather than incidence.
Mobility status was recorded at the evaluation time-point and classified as semi-mobile (able to change position with assistance and/or limited ambulation) or immobile (bedbound and unable to reposition without full assistance), as documented in home-care assessment records.
Feeding route at the evaluation time-point was categorized as oral, nasogastric tube (NG), or percutaneous endoscopic gastrostomy (PEG) based on the clinical record and was interpreted as an indicator of care dependency rather than a distinct nutritional exposure.
Laboratory variables included hemoglobin (g/dL), serum albumin (g/L), and CRP (mg/dL). “Same-day” laboratory measurements were defined as albumin and CRP results recorded on the same calendar date in the laboratory record. The CRP-to-albumin ratio (CAR) was calculated using these same-day values. The Norton score was extracted as the value documented at the evaluation time-point. In the institutional home-care protocol, patients receive scheduled home visits every two weeks, and a Norton assessment is performed at each visit. Additional visits may occur for clinical indications (e.g., wound care, clinical deterioration); Norton scores are also recorded during these unscheduled visits. Although the standard schedule is biweekly, actual visit frequency may vary by clinical need; therefore, we used the Norton score documented at the cross-sectional evaluation time-point for all analyses.
Statistical analysis
Continuous variables were summarized as mean ± standard deviation or median (interquartile range), and categorical variables as counts and percentages. Group comparisons were performed using the independent-samples t test or Mann–Whitney U test for continuous variables, and the chi-square test or Fisher’s exact test for categorical variables, as appropriate. Because of small subgroup sizes for non-oral feeding routes (NG/PEG), subgroup-specific estimates were interpreted descriptively and counts were reported alongside percentages.
Receiver operating characteristic (ROC) analyses were used to evaluate discrimination, and results were reported as area under the curve (AUC) with 95% confidence intervals. Multivariable logistic regression was used to examine associations with pressure ulcer presence, and model calibration was assessed using the Hosmer–Lemeshow goodness-of-fit test. Analyses were conducted using a complete-case approach (participants with missing values in variables required for a given analysis were excluded from that analysis). A two-sided p value < 0.05 was considered statistically significant.
Ethics
The study was approved by the institutional ethics committee (Decision No: 2025/18); informed consent was waived due to the retrospective design. The study is reported in accordance with the STROBE statement.
Results
A total of 328 patients were included in the analysis. The mean age was 77.8 ± 15.0 years, and 68.6% were female. Overall, 66.5% of patients were semi-mobile and 33.5% were completely immobile. Most patients (97.3%) were fed orally, whereas 0.9% (n = 3) received enteral nutrition via nasogastric (NG) tube and 1.8% (n = 6) via percutaneous endoscopic gastrostomy (PEG). The mean hemoglobin level was 11.8 ± 1.9 g/dL, mean serum albumin level was 37.9 ± 4.5 g/L, and mean Norton score was 14.4 ± 2.7.
The study population comprised 328 patients, and the overall prevalence of pressure ulcer presence at the evaluation time-point was 8.2% (27/328) (Table 1).
Table 1.
Demographic and clinical characteristics of the study population and distribution of pressure ulcers
| Characteristic | Total (N = 328) | No ulcer (n = 301) | Ulcer (n = 27) | Ulcer (%) |
|---|---|---|---|---|
| Sex, n (%) | ||||
| Male | 103 (31.4) | 95 | 8 | 7.8 |
| Female | 225 (68.6) | 206 | 19 | 8.4 |
| Mobility, n (%) | ||||
| Semi-mobile | 218 (66.5) | 209 | 9 | 4.1 |
| Immobile | 110 (33.5) | 92 | 18 | 16.4 |
| Feeding route, n (%) | ||||
| Oral | 319 (97.3) | 297 | 22 | 6.9 |
| Nasogastric (NG) | 3 (0.9) | 1 | 2 | 66.7 |
| PEG | 6 (1.8) | 3 | 3 | 50.0 |
Values are presented as n (%)
NG Nasogastric, PEG Percutaneous endoscopic gastrostomy
The C-reactive protein to albumin ratio (CAR) was not normally distributed in either group (Shapiro–Wilk p < 0.001). Therefore, CAR values were compared using the Mann–Whitney U test and are presented as median (IQR). CAR was significantly higher in patients with pressure ulcers than in those without pressure ulcers (0.421 [0.61] vs. 0.157 [0.38]; Mann–Whitney U = 2748, Z = − 2.787; p = 0.005). The C-reactive protein to albumin ratio (CAR) demonstrated statistically significant but only modest discriminatory ability for pressure ulcer presence, with an area under the curve (AUC) of 0.662 (SE 0.053; 95% CI 0.559–0.765; p = 0.005).
When patients were compared according to the presence of pressure ulcers, serum albumin levels were significantly lower in the ulcer group than in the non-ulcer group (35.8 ± 4.1 vs. 38.0 ± 4.5 g/L; p = 0.015; Cohen’s d = 0.49). Norton scores were also lower in patients with ulcers (12.3 ± 2.5 vs. 14.6 ± 2.6; p < 0.001; Cohen’s d = 0.87). Hemoglobin levels were similar between groups (ulcer: 11.5 ± 2.0 vs. no ulcer: 11.8 ± 1.9 g/dL; p = 0.434) (Table 2).
Table 2.
Comparison of laboratory and risk assessment parameters between patients with and without pressure ulcers
| Variable | No ulcer (n = 301) Mean ± SD | Ulcer (n = 27) Mean ± SD | p value | Effect size |
|---|---|---|---|---|
| Albumin (g/L) | 38.0 ± 4.5 | 35.8 ± 4.1 | 0.015 | d = 0.49 |
| Norton score | 14.6 ± 2.6 | 12.3 ± 2.5 | < 0.001 | d = 0.87 |
| Hemoglobin (g/dL) | 11.8 ± 1.9 | 11.5 ± 2.0 | 0.434 | n.s. |
Values are presented as mean ± standard deviation
Between-group comparisons were performed using the independent samples Student’s t-test
SD Standard deviation, n.s. Not significant
In categorical analyses, pressure ulcer prevalence was higher in immobile patients than in semi-mobile patients (16.4% vs. 4.1%; χ² (1) = 14.49, p < 0.001).
Receiver operating characteristic (ROC) analysis showed that the inverse serum albumin variable (InvAlb) yielded an AUC of 0.659 (95% CI, 0.561–0.757; p = 0.006) for pressure ulcer presence.Based on ROC analysis within this dataset, an albumin value of 31.5 g/L corresponded to a sensitivity of 81.5% and a specificity of 92.6%; this threshold should be considered exploratory and not a validated clinical decision cutoff.
Pressure ulcer prevalence differed significantly according to feeding route (χ² (2) = 28.170, p < 0.001). The prevalence was 6.9% (22/319) in orally fed patients, 66.7% (2/3) in NG-fed patients, and 50.0% (3/6) in PEG-fed patients. The Fisher–Freeman–Halton exact test and Monte Carlo simulation confirmed the significance of this association (exact p < 0.001; Monte Carlo two-sided p = 0.001; 99% CI, 0.000–0.002) (Table 3). However, the number of patients receiving NG or PEG feeding was small; therefore, subgroup-specific prevalence estimates and effect size interpretations should be made cautiously. Because of small subgroup sizes, estimates for NG and PEG feeding should be interpreted descriptively, and inferential conclusions are limited.
Table 3.
Relationship between feeding route and presence of pressure ulcers
| Feeding route | No ulcer n (%) | Ulcer n (%) | Total (N) |
|---|---|---|---|
| Oral | 297 (93.1) | 22 (6.9) | 319 |
| NG | 1 (33.3) | 2 (66.7) | 3 |
| PEG | 3 (50.0) | 3 (50.0) | 6 |
Pearson chi-square: χ² (2) = 28.170, p < 0.001
Fisher–Freeman–Halton exact test and Monte Carlo simulation were applied due to small expected cell counts (two-sided p = 0.001)
NG Nasogastric, PEG Percutaneous endoscopic gastrostomy
Spearman correlation analysis showed a weak but statistically significant negative correlation between serum albumin level and pressure ulcer stage (ρ=–0.153, p = 0.006), indicating lower albumin levels in patients with more advanced-stage ulcers. Given the cross-sectional design, this correlation reflects co-occurrence at assessment rather than temporal direction. CRP levels were higher in patients with pressure ulcers, as demonstrated by the Mann–Whitney U test (U = 2830.000, Z=–2.613, p = 0.009); the mean rank of CRP was 210.19 in the ulcer group and 160.40 in the non-ulcer group.
In multivariable logistic regression analysis including feeding route, mobility status, and serum albumin level, feeding route and mobility were independently associated with pressure ulcer presence at the evaluation time-point. Hemoglobin was tested in the between-group comparison and was not significantly different between patients with and without pressure ulcers (p = 0.434); therefore, hemoglobin was not included in the final multivariable model (Table 2). In multivariable logistic regression, with non-oral feeding (NG/PEG) as the reference category, oral feeding was associated with significantly lower odds of pressure ulcers (OR 0.116, 95% CI 0.028–0.481; p = 0.003). Likewise, with immobility as the reference, semi-mobile patients had significantly lower odds of pressure ulcers compared with immobile patients (OR 0.291, 95% CI 0.121–0.700; p = 0.006). Serum albumin level showed a trend toward an inverse association, but this did not reach statistical significance after adjustment (OR 0.927 per 1 g/L increase, 95% CI 0.854–1.006; p = 0.069) (Table 4).
Table 4.
Multivariable logistic regression analysis for pressure ulcer presence
| Predictor | B | SE | Wald χ² | OR (Exp[B]) | 95% CI for OR | p value |
|---|---|---|---|---|---|---|
| Non-oral feeding (NG/PEG) vs. Oral | -2.158 | 0.727 | 8.803 | 0.116 | 0.028–0.481 | 0.003 |
| Serum albumin (g/L) | -0.076 | 0.042 | 3.309 | 0.927 | 0.854–1.006 | 0.069 |
| Immobile vs. Semi-mobile | -1.235 | 0.448 | 7.599 | 0.291 | 0.121–0.700 | 0.006 |
Model constant: B = 3.041, SE = 1.624, p = 0.061
Dependent variable: Pressure ulcer presence (PU: 1 = ulcer, 0 = no ulcer)
Feeding route coded as 0 = Oral (reference), 1 = Non-oral (NG/PEG)
Mobility coded as 0 = Semi-mobile (reference), 1 = Immobile
The combined multivariable model yielded an AUC of 0.760 (SE 0.049; 95% CI 0.663–0.857; p < 0.001) (Fig. 1). Model calibration was assessed using the Hosmer–Lemeshow goodness-of-fit test (χ²=9.088, df = 8; p = 0.335).
Fig. 1.
ROC curve of the multivariable model for predicting pressure ulcer presence. Receiver operating characteristic curve based on predicted probabilities from the logistic regression model including feeding route (non-oral vs. oral), mobility status (immobile vs. semi-mobile), and serum albumin level. The model yielded an AUC of 0.760 (95% CI 0.663–0.857; p < 0.001)
Discussion
In this home-care cohort, pressure ulcer presence at the evaluation time-point was 8.2%. Patients with pressure ulcers had lower serum albumin levels, reduced mobility, and higher CRP and CAR values compared with those without pressure ulcers. Pressure ulcer presence also differed by feeding route; however, because very few patients were receiving non-oral feeding (NG/PEG), this variable should be interpreted primarily as a marker of advanced care dependency/frailty and the subgroup-specific estimates should be considered descriptive.
The observed prevalence is broadly consistent with reports from acute care, intensive care, neurocritical care, and long-term care settings, where pressure ulcers remain prevalent despite prevention efforts [16].
Although direct comparisons across settings should be interpreted with caution, mobility limitation is repeatedly emphasized as a dominant risk factor across different populations [13]. Conceptually, immobility contributes to sustained pressure and shear forces, impaired tissue perfusion, and reduced tissue tolerance; narrative reviews and synthesis literature support the central role of mobility-related mechanisms and multifactorial risk pathways in pressure ulcer development [17, 18].
Patients with pressure ulcers had lower serum albumin levels compared with those without ulcers. Previous literature has long discussed the relationship between nutrition and pressure ulcers, emphasizing that malnutrition contributes to impaired tissue integrity maintenance and repair [5]. Systematic reviews and clinical guidelines support nutritional assessment and, when indicated, nutritional interventions as part of prevention and treatment bundles [2, 12, 14]. Experimental studies also suggest that adequate protein intake supports key wound-healing processes, including collagen synthesis and tissue repair [8]. Observational studies in clinical populations have reported associations between low albumin levels and pressure ulcer risk [19], and intensive care–focused studies have examined albumin-centered approaches in greater detail [20]. However, serum albumin is influenced by inflammation and disease severity, therefore, our findings should be interpreted as associative rather than as evidence of a specific causal nutritional mechanism. In addition, any albumin threshold derived from ROC analysis in this study (e.g., 31.5 g/L) represents an internally derived, exploratory cut-point for discrimination within this sample. It is not intended to provide clinical guidance or to define a prevention/triage threshold, and it should not be used operationally without external validation.
Albumin is best interpreted as part of a broader vulnerability profile—including dependency, immobility, and inflammation—that can trigger intensified prevention bundles rather than as a standalone nutritional target [3, 9].
Feeding route is clinically relevant, as enteral feeding via nasogastric tube or percutaneous endoscopic gastrostomy often reflects advanced comorbidity burden, dysphagia, frailty, and high care dependency—features that may coexist with an increased risk of pressure ulcers [5]. Patterns and outcomes related to feeding tube use in hospitalized older populations similarly support the notion that feeding route may serve as a marker for illness severity and dependency [21]. Studies in home-care and palliative-care settings have also emphasized nutrition-related and care-dependency factors within pressure ulcer risk profiles [22, 23]; in our cohort, non-oral feeding (NG/PEG) is best interpreted as a marker of advanced care dependency/frailty (i.e., frail patients may require enteral support), and given the very small NG/PEG subgroup sizes this observation should be interpreted descriptively. However, the number of patients receiving NG or PEG feeding in our cohort was small; and is too limited to support subgroup-specific inference; therefore, these estimates are reported descriptively without drawing conclusions. The principal implication is that non-oral feeding in this setting should be understood not as a precise quantitative measure of risk attributable to individual enteral feeding modalities, but rather as a marker of high care dependency and frailty.
Our findings, aligned with evidence that the risk factors for community-acquired pressure ulcers differ from those for hospital-acquired ulcers, highlight the need for risk-assessment approaches in community and home-care settings that accurately reflect patient dependency and functional limitations [3].
Inflammatory markers also differed between groups. Patients with pressure ulcers had higher CRP and CAR values, and CAR demonstrated modest discriminative ability. Biomarker-focused evidence—including systematic reviews, meta-analyses, and geriatric biomarker studies [24, 25]—supports an association between physiological stress or inflammation and pressure ulcer risk or early detection; however, performance and clinical utility vary across settings. In hospitalized older populations, CAR has been evaluated as a prognostic marker independent of diagnosis, underscoring its role as a composite indicator of inflammation and nutritional reserve [24]. Consistent with our AUC estimates, CAR should be regarded not as a standalone screening or decision-making tool in home-care or primary care practice, but rather as a complementary marker with modest discriminative value. In a primary care–led home-care context, CAR may be reviewed alongside mobility and care-dependency indicators as a complementary marker of inflammatory burden. However, serum albumin is strongly influenced by inflammation, illness severity, hydration status, and other non-nutritional factors; therefore, neither albumin nor CAR should be used to guide resource prioritization or as a standalone marker of nutritional status without external validation [3, 9].
In the multivariable analysis, mobility status and feeding route remained independently associated with the presence of pressure ulcers, whereas serum albumin demonstrated a statistically non-significant trend after adjustment. This pattern is consistent with broader evidence indicating that pressure ulcer risk is multidimensional, and that functional status and care-dependency variables may exert a dominant influence when modeled alongside laboratory parameters [12, 13, 26, 27]. Recent studies have also emphasized risk modeling and prediction approaches for pressure ulcers; however, such models typically require careful validation and context-specific application [28, 29]. Accordingly, although our combined model yielded an AUC of 0.760 within this cohort, it should be interpreted as an internally evaluated associative model rather than as a clinically ready predictive tool, and external validation is required before any clinical application. For example, in a Japanese home-care setting, Kohta et al. reported an AUC of 0.737 for the PPRA-Home scale, with AUCs of 0.814 for the Braden scale and 0.794 for the Ohura-Hotta scale in discriminating between individuals with and without pressure ulcer. Taken together, these findings suggest that discrimination estimates in this field are often moderate and setting-dependent, reinforcing the need for external validation before operational use [30].
Several limitations should be acknowledged. First, analyses were conducted in a single cohort without external validation; therefore, generalizability cannot be assumed, and model discrimination should be interpreted cautiously. Second, the cross-sectional observational design precludes causal inference. Third, the small number of patients in the NG and PEG subgroups may limit the precision of feeding route–related estimates; this is a common issue in real-world cohorts in which feeding tube use is relatively infrequent but clinically meaningful [16, 21, 22, 31]. Finally, external studies include a range of inpatient and long-term care settings, including neurosurgical cohorts and acutely hospitalized populations; risk structures in these contexts may differ from those in home-care settings, reinforcing the need for setting-specific interpretation [13, 32, 33]. In addition, community-based studies highlight that pressure ulcers in primary care populations are associated with a substantial symptom burden, including pain, underscoring the importance of prevention-oriented care pathways and consistent documentation within primary care services [4, 9].
Despite these limitations, the findings contribute to the literature by characterizing mobility, nutrition-related indicators, feeding route, and inflammation in a real-world home-care population. The results are directionally consistent with guideline recommendations emphasizing comprehensive risk assessment, optimization of mobility, and nutritional monitoring for the prevention and management of pressure ulcers [2, 10, 12]. Taken together, these results support a primary care–relevant interpretation in which functional dependency—particularly reduced mobility—is associated with pressure ulcer presence, while inflammation–nutrition markers may provide complementary clinical context [3, 9]. Given the very small NG/PEG subgroup sizes, feeding route should be interpreted descriptively as a marker of care dependency rather than as a basis for operational triage.
At a population level, these exploratory associations may help frame future research on prevention approaches in home-care services, but they should not be interpreted as actionable service-planning recommendations without external validation.This approach aligns with broader public health goals of reducing avoidable complications and optimizing resource use in ageing populations receiving long-term home-based care.
Strengths and limitations
Strengths
This study focuses on a primary care–led home-care population, a setting that remains underrepresented in the pressure ulcer literature compared with inpatient and institutional cohorts.
The analysis integrates functional status (mobility), care-dependency indicators (feeding route), and inflammation/nutrition-related markers, and, given the limited number of events, we restricted the multivariable model to a small set of clinically interpretable variables to minimize overfitting risk.
Limitations
This was a single-cohort, retrospective, cross-sectional study; therefore, temporal relationships and causality cannot be inferred, and generalizability is limited.
External validation of ROC-based discrimination estimates and the multivariable model was not performed; thus, model performance should be considered exploratory and may not replicate in other home-care cohorts.
Inclusion required availability of same-day laboratory results and documented risk assessment at the cross-sectional assessment time point, which may have introduced selection bias toward patients under closer monitoring and may have influenced both prevalence estimates and associations.
The number of patients receiving NG/PEG feeding was small, limiting precision and potentially producing unstable subgroup-specific estimates; feeding route should therefore be interpreted primarily as a marker of frailty and care dependency rather than a direct causal exposure.
Pressure ulcer presence and staging were derived from retrospective nursing documentation, which may introduce information bias/misclassification, and serum albumin has limited specificity as a nutritional marker because it is influenced by systemic inflammation and illness severity.
Although penalized regression methods may offer advantages in small-event settings, the present analyses should be interpreted as exploratory.
This inclusion strategy may have preferentially selected patients under closer clinical surveillance, potentially influencing prevalence estimates and observed associations.
Conclusion
In this cohort of home-care patients with limited mobility, pressure ulcer presence was associated with immobility, non‑oral feeding routes, lower serum albumin levels, and greater inflammatory burden. CAR and inverse albumin showed only modest discriminatory performance, and the multivariable model demonstrated moderate discrimination; however, these estimates are exploratory and derived from a single cross‑sectional sample. As such, neither CAR, albumin thresholds, nor the multivariable model should be used as standalone clinical tools, and any cutoffs identified here are dataset‑specific and not clinically validated. Overall, the findings reinforce the importance of integrated, comprehensive risk assessment—including functional status, nutrition‑related indicators, and markers of systemic inflammation—in home‑care settings, in line with current prevention frameworks.
Acknowledgements
The authors thank Nurse Zeynep Kartal for her assistance during the data collection phase of this study.
Authors’ contributions
Conceptualization – MKO; Study design – MKO, OE, EO; Data collection – MKO, LMY, EO, OE; Statistical analysis – MKO, LMY, EO, OE, DCO; Interpretation of data – MKO, LMY, EO, OE; Drafting of the manuscript – MKO, DCO; Critical revision of the manuscript – MKO, LMY, EO, OE, DCO; Final approval – MKO, LMY, EO, OE, DCO; Accountability – MKO, LMY, EO, OE.
Funding
This study received no external funding.
Data availability
The data presented in this study are available on request from the corresponding author. The data are not publicly available due to privacy and ethical restrictions.
Declarations
Ethics approval and consent to participate
The study was conducted in accordance with the Declaration of Helsinki and was approved by the Ordu University Clinical Research Ethics Committee (Decision No: 2025/18). Due to the retrospective design, informed consent was waived.
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
The data presented in this study are available on request from the corresponding author. The data are not publicly available due to privacy and ethical restrictions.