Fracture Type Heterogeneity May Dilute the Prognostic Signal of Preoperative Hemoglobin Decline in Hip Fracture Patients

Dear Editor,

1.

Graif and colleagues deserve commendation for their large retrospective cohort study examining whether preoperative hemoglobin decline independently predicts mortality in older hip fracture patients [1]. The systematic evaluation of six Hb‐drop thresholds and the consistent null findings across multiple time points represent a methodologically rigorous approach. However, the authors' analysis treats hip fractures as a homogeneous entity, overlooking a key anatomical distinction that may fundamentally affect the interpretation of their findings.

Hip fractures encompass distinct fracture types with markedly different bleeding profiles. Intracapsular femoral neck fractures occur in a closed space with limited blood loss, whereas extracapsular intertrochanteric and subtrochanteric fractures involve highly vascularized cancellous bone and surrounding soft tissues, resulting in substantially greater hemorrhage [2]. This anatomical reality is reflected in quantifiable differences in preoperative hemoglobin decline. Harper and colleagues reported that extracapsular fractures had a median Hb drop of 1.1 g/dL compared with 0.6 g/dL for intracapsular fractures (p = 0.027), with extracapsular fractures requiring preoperative transfusion four times more frequently [2]. Similarly, Kamiloski and Kasapinova demonstrated a clear gradient: Hb drop was lowest in femoral neck fractures (6.1 g/L), intermediate in intertrochanteric fractures (12.05 g/L), and highest in subtrochanteric fractures (16.52 g/L), with statistically significant differences between groups [3]. Stacey and colleagues further confirmed that fracture type is an independent predictor of Hb drop (p = 0.02) [4]. Even within intertrochanteric fractures, instability is associated with greater Hb decline [5]. Collectively, these findings indicate that preoperative Hb drop is substantially influenced by fracture type, a variable notably absent from the authors' multivariate models.

By pooling all fracture types together without adjustment, the authors may have inadvertently diluted the prognostic signal of Hb decline. Extracapsular fractures have higher baseline mortality risk and greater blood loss [6], contributing a stronger Hb‐drop signal; intracapsular fractures, with less bleeding and lower mortality, contribute a weaker one. The result of averaging across these heterogeneous groups could be a null finding that masks fracture‐specific associations. The authors' finding that admission Hb was not independently associated with mortality (OR 1.64, 95% CI 0.79–3.43, p = 0.187) also warrants re‐evaluation in light of fracture type. Admission Hb may have different meanings across fracture types: for intracapsular fractures, it may approximate pre‐fracture baseline and reflect chronic health status; for extracapsular fractures, it may already reflect acute blood loss sustained before arrival. This distinction is clinically meaningful because the mechanisms linking Hb to mortality differ fundamentally: low Hb from chronic disease signals diminished physiological reserve, whereas acute Hb decline from hemorrhage signals ongoing blood loss and hemodynamic stress. Recent evidence confirms that chronic preinjury anemia is independently associated with 1‐year mortality in geriatric hip fracture patients [7]. Admission Hb ≤ 10 g/dL increases 1‐year mortality risk by 76% [8]. In a more detailed analysis, a large cohort study of 2589 patients demonstrated a nonlinear relationship between admission Hb and 3‐year mortality [9]. The inflection point was at 9.8 g/dL. Below this threshold, mortality risk increased substantially (HR 0.81, 95% CI 0.74–0.89, p < 0.0001); above it, no additional risk was observed. These findings support the view that admission Hb captures baseline physiological reserve rather than merely acute blood loss. If the contribution of fracture type is not accounted for, the relationship between admission Hb and mortality may be obscured.

We suggest three refinements for future analyses. First, conduct subgroup analyses stratified by fracture type (intracapsular vs. extracapsular) to evaluate whether the association between Hb decline and mortality differs across these anatomically distinct groups. Second, include fracture type as a covariate in multivariate models to assess whether it confounds or modifies the Hb‐mortality relationship. Third, interpret admission Hb in light of its likely meaning: Baseline physiological reserve for intracapsular fractures versus post‐injury status for extracapsular fractures, rather than treating it as a uniform baseline across all patients. Our comments are intended to refine the interpretability of this otherwise valuable contribution, rather than to diminish its overall significance.

Author Contributions

B.H. conceived the letter concept, performed the literature analysis, and drafted the manuscript. H.D. critically revised the manuscript for important intellectual content and provided supervision. All authors approved the final version and agree to be accountable for all aspects of the work.

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Data Availability Statement

Data sharing not applicable to this article as no datasets were generated or analysed during the current study.