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TL;DR: A meta-analysis of observational cohorts links a higher admission glucose-to-potassium ratio (GPR, also called the stress index) with increased mortality and poor functional outcome after traumatic brain injury (TBI). The evidence is observational and heterogeneous, so this is a promising bedside prognostic signal, not an established clinical tool.
Traumatic brain injury remains a leading cause of death and long-term disability. Clinicians currently rely on clinical scores and radiologic findings to estimate early risk, and researchers have been looking for simple, inexpensive markers that add information to these tools. The glucose-to-potassium ratio is one such candidate. It combines two routine admission laboratory values: stress hyperglycemia (elevated blood glucose) and hypokalemia (low potassium). Both reflect the body's systemic stress response, and the ratio is calculated from a standard blood panel that is available in most emergency settings.
This PRISMA-guided systematic review and meta-analysis pooled observational cohort studies of adults aged 18 and older with CT-confirmed TBI. The authors assessed two types of outcomes: mortality, and functional or "poor" outcome as defined by each included study. Pooled estimates used random-effects models, with odds ratios (ORs) for dichotomous outcomes and mean differences (MDs) for continuous GPR values. Heterogeneity was quantified with I², and the authors ran subgroup, leave-one-out, and fixed-versus-random sensitivity analyses along with funnel-plot inspection.
For mortality, three studies (4,550 patients in total) compared high versus low GPR. High GPR was associated with markedly increased odds of death (pooled OR 11.97, 95% CI 2.68 to 53.37; p = 0.001; I² = 88%). The confidence interval is very wide and heterogeneity is high, so the magnitude of this estimate should be read with considerable caution. Across four studies, patients with poor outcomes had higher admission GPR than those with good outcomes (pooled MD 16.82, 95% CI 12.70 to 20.94; p < 0.00001; I² = 61%). In five studies evaluating GPR as a prognostic predictor, the pooled adjusted OR for adverse outcome was 2.10 (95% CI 1.51 to 2.93; p < 0.0001; I² = 37%), a more moderate and more consistent estimate.
Heterogeneity was partly explained by sample size. Effects were larger in small single-center cohorts and more modest, though still statistically significant, in the large registry-based study. Funnel-plot asymmetry suggested possible small-study effects and publication bias, which means smaller positive studies may be overrepresented in the literature and could inflate pooled estimates. The authors themselves emphasize that the evidence is observational and that standardized thresholds have not been validated.
This is primarily a clinical research finding aimed at emergency and neurocritical care teams, not a recommendation for individuals. Several points are worth keeping in mind:
| Field | Detail |
|---|---|
| Study type | Systematic review and meta-analysis (PRISMA-guided) |
| Population | Adults (18 years and older) with CT-confirmed TBI |
| Total sample | 4,550 patients across included studies |
| Exposure | Admission glucose-to-potassium ratio (GPR / stress index) |
| Outcomes | Mortality; functional or poor outcome |
| Key estimates | OR 11.97 (mortality); MD 16.82 (outcome GPR); adjusted OR 2.10 (prognostic) |
| Analysis | Random-effects models; I²; subgroup, leave-one-out, and funnel-plot analyses |
| Evidence level | Observational cohorts, pooled; heterogeneous; possible publication bias |
| Journal | Frontiers in Neurology |
| PubMed ID | 42889002 |
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