Hyperglycemia and Outcomes after Acute Traumatic Spinal Cord Injury: Scoping Review

Abstract

Hyperglycemia is a recognized prognostic marker in neurocritical care, but condition-specific data and glycemic targets for traumatic spinal cord injury (TSCI) remain undefined. We conducted a scoping review to map how early hyperglycemia has been defined and measured in adults with acute TSCI and how it relates to neurological and functional outcomes. Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses for scoping reviews guidance, PubMed, Embase, and Scopus were searched from inception to November 2025 for studies enrolling adults (≥18 years) within 7 days of TSCI, defining hyperglycemia at ≥126 mg/dL, and reporting neurological, functional, or mortality outcomes. Eligible designs included prospective and retrospective cohorts and registry-based analyses; pediatric, diabetic-only, nontraumatic, animal, and chronic-phase studies were excluded. Of 2323 records, 6 observational studies (n = 2586) met the inclusion criteria. Most cohorts involved predominantly cervical injuries and used admission or 24-h glucose as the primary exposure. Across studies, more severe neurological impairment at presentation was associated with higher admission glucose, and admission hyperglycemia was generally linked to poorer motor recovery, lower Spinal Cord Independence Measurement scores, and unfavorable AIS profiles at discharge, although these associations frequently attenuated after multivariable adjustment. Overall, evidence on hyperglycemia in acute TSCI is limited, heterogeneous, and observational. Early hyperglycemia shows signals of association with adverse neurological and functional outcomes, but effect estimates are inconsistent and do not support specific glycemic targets. Glucose and composite indices remain candidate prognostic biomarkers that require validation in standardized, prospective multicenter cohorts before interventional trials can be justified.

Keywords

functional outcomes hyperglycemia scoping review spinal cord injury

Introduction

Traumatic spinal cord injury (TSCI) remains a major cause of long-term disability worldwide.¹ Survivors frequently face persistent neurological impairment, functional limitations, and secondary medical complications that extend well beyond the acute hospitalization. The rehabilitation phase is intensive, requiring weeks of inpatient therapy followed by long-term outpatient support, and many patients continue to struggle with restrictions in mobility, independence, and community participation.^2,3 These challenges are accompanied by reduced health-related quality of life (HRQoL) and common psychosocial difficulties. Collectively, this burden underscores the enduring impact of spinal cord injury (SCI) on individuals and health systems alike and highlights the importance of ongoing efforts to optimize early management strategies.

Acute dysglycemia has been a clinically important factor in neurocritical care. This relationship appears particularly pronounced in patients with neurological injury, where the central nervous system demonstrates heightened vulnerability to metabolic disturbances. In traumatic brain injury (TBI), for example, higher glucose levels have been associated with unfavorable neurological outcomes, while attempts at aggressive insulin therapy have not improved survival and carry a clear risk of hypoglycemia.⁴ Similar observations extend across broader neurocritical cohorts, where early hyperglycemia has been identified as a predictor of poor prognosis, reinforcing the notion that glycemic balance in these patients is both fragile and clinically consequential.⁵ Together, these findings highlight the central role of glucose as a modifiable physiological marker in neurological injury while underscoring the complexity of defining optimal targets for management. Across general intensive care and neurocritical populations, glycemic management has been evaluated in numerous randomized controlled trials, reflecting sustained interest in glucose as a clinically important physiological domain.^4,6 By contrast, TSCI lacks condition-specific trials or inpatient glycemic targets. Contemporary guidance emphasizes early surgical decompression (≤24 h) and targeted mean arterial pressure augmentation to support cord perfusion but is silent on glucose control, so bedside practice typically follows general ICU ranges.^7–9 Within this framework, glycemic management remains an under-examined, potentially modifiable domain in acute SCI that warrants systematic evaluation on its own terms.

Our objective was to map, among adults with acute TSCI, the reported associations between early hyperglycemia and clinical outcomes within the acute phase. We also wanted to describe the study designs, exposure definitions, and time windows in the literature.

Methods

Search strategy

The scoping review conducted was in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses for scoping reviews.¹⁰ This review was not formally registered, as protocol registration was not required. A systematic search was conducted in PubMed, Embase, and Scopus from database inception through November 2025 of the final search. The search terms used were: #1

“Spinal Cord Injury” OR “Spinal Cord Trauma” AND “hyperglycemia” OR “hyperglycaemia” OR “glycemic control” and

“hyperglycemia” OR “glucose” OR “blood sugar” OR “dysglycemia” AND “acute” AND “spinal cord injury” OR “spinal cord trauma” OR “traumatic spinal cord contusion”

No restrictions on publication date or language were applied. Reference lists of all included articles were reviewed to identify additional eligible studies.

Eligibility criteria

Studies were included if they examined adults, defined as individuals aged 18 years or older, with acute TSCI defined as within 7 days. Hyperglycemia had to be defined by a threshold of at least 126 mg/dL, with measurement occurring in the acute period. The primary outcomes of interest were neurological outcomes. Secondary outcomes included functional outcomes, in-hospital mortality, or mortality at 90 days or at 1 year. Eligible designs included prospective and retrospective cohort studies, registry-based analyses, and randomized controlled trials. Exclusion criteria included pediatric cohorts, diabetic specific cohorts, non-TSCI unless data for traumatic cases were reported separately, case series with fewer than 10 patients, animal or laboratory studies, and reports limited to chronic-phase or outpatient populations.

Study selection and data extraction

Titles, abstracts, and full texts were screened independently by two reviewers (M.C., K.M.) within Covidence systematic review software. Duplicate records were identified automatically by Covidence and then verified by the reviewers. Disagreements were resolved by consensus or by consultation with a third reviewer (J.V.). Data extraction was carried out using a standardized form that recorded study design, sample size, patient demographics, definition and timing of hyperglycemia, comparator definition, and outcomes measured. Where effect sizes were not reported, raw data were extracted when available. Two records could not be retrieved after manually searching for full-text review because one corresponded to a clinical trial registration without a published results article, whereas the other was available only as a conference abstract with no full-text article identified.

Result

Demographics

From Scopus, Embase, and PubMed, 2323 records were identified. After removing 118 duplicates, 2205 titles/abstracts were screened; 25 full texts were assessed for eligibility, and 6 studies met the inclusion criteria (Fig. 1; Table 1).^10–15 All identified studies included were observational, with a combined cohort of 2586 patients with acute TSCI. Across studies reporting admission ASIA impairment (AIS) grade, the most common category was complete injury (AIS A) with a pooled total of 206 patients.^10,13 Falls were the predominant mechanism of injury, with an estimated 776 patients across cohorts (35%).^{10,11,13–15} Cervical spinal cord injury was the most frequent anatomical level, with an estimated 1484 cervical injuries reported across five cohorts (67.3%).^{10,11,13–15} One study did not include a normoglycemic comparator group and only reported outcomes within a hyperglycemic spinal cord injury population.¹⁵

FIG. 1.

PRISMA 2020 flow diagram illustrating the study selection process for the scoping review. PRISMA, Preferred Reporting Items for Systematic Reviews and Meta-Analyses.

Table 1.

Characteristics of Studies

Article	Study design	Cohort	Outcomes	Time frame	Threshold glucose	Mean glucose(SD)	Collected glucose	Conclusion
Kazu et al. (2014)¹¹	RC	206	AIS	In-hospital	≥126 mg/dL	166 ± 4.0 mg/dL	Admiss.	In acute SCI patients admitted within 24 h, admission hyperglycemia (≥126 mg/dL) was associated with a higher proportion of poor AIS outcomes, lower ASIA motor scores, lower motor recovery rates, and lower SCIM scores at discharge; on multivariable analysis, higher admission glucose remained an independent predictor of worse motor outcome
Park et al. (2020)¹²	RC	66	AIS	Admiss. to 1 year	≥150 mg/dL	160.0 ± 9.0 mg/dL	Admiss.	In patients with acute cervical SCI, higher preinjury HbA1c (≥6.5%) independently predicted poor functional recovery (less AIS grade improvement), and patients with chronic hyperglycemia had higher CSF IL-6/IL-8 levels after injury, suggesting chronic dysglycemia before SCI is a negative prognostic factor
Torbati et al. (2015)¹³	CS	380	Motor Force (MF)	In-hospital	≥126 mg/dL	142.6 mg/dL	Admiss.	Among traumatic SCI patients, higher admission blood glucose correlated with greater motor deficit severity, and in those with marked hyperglycemia (>200 mg/dL), insulin treatment and glucose control were associated with significant improvement in motor force between admission and discharge
Zhou et al. (2023)¹⁴	RC	520	AIS	Admiss. to 6 months follow-up	NR	143.9 ± 20.7 mg/dL	Admiss.	Higher admission serum glucose/potassium ratio was associated with more severe initial AIS grade and poorer 6-month AIS outcome; GPR remained an independent predictor of poor prognosis with good discrimination
Tee et al. (2014)¹⁵	RC	915	HRQoL: SF-12	1 year	>144 mg/dL	NR	48 h	In polytrauma patients with spine injuries, early hyperglycemia (>8 mmol/L within 48 h) independently predicted suboptimal 1-year physical HRQoL (SF-12 PCS), along with tachycardia, multiple comorbidities, and thoracic injuries; no early predictors were identified for mental HRQoL
Furlan (2021)¹⁶	RC	499	NASCIS motor, sensory	6 weeks, 6 months, and 1 year	>140 mg/dL	188.2 ± 2.3 mg/dL	24 h	In the NASCIS-3 cohort, hyperglycemia at day 7 after acute traumatic SCI was associated with higher 1-year mortality, and persistent hyperglycemia to day 7 correlated with lower functional (FIM) scores, whereas hyperglycemia in the hyperacute phase (24–48 h) was not significantly associated with neurological recovery
			Functional Independence Measurement (FIM)	6 weeks, 6 months, and 1 year	>180 mg/dL	164.4 ± 2.1 mg/dL	48 h
			Functional Independence Measurement (FIM)	6 weeks, 6 months, and 1 year	>180 mg/dL	125.0 ± 2.3 mg/dL	7 days

Admiss., admission; AIS, ASIA Impairment Score; CS, cross-sectional cohort; HRQoL, health-related quality of life; NASCIS, National Acute Spinal Cord Injury Studies; NR, not reported; RC, retrospective cohort; SCIM, Spinal Cord Independence Measurement; SF-12, Short Form 12–Questionnaire Health Survey.

Neurological severity

Patients with more severe neurological deficits at presentation tended to have higher admission glucose. In one cohort, admission glucose was higher in patients presenting with more severe impairment (AIS A–C) compared with those presenting with less severe deficits (AIS D), with median values of 138 mg/dL [116.5–169.5] versus 120.5 mg/dL [102.5–140.5].¹¹ In another cohort, weaker motor function on examination was associated with higher glucose at presentation: patients with 0/5, 1/5, 2/5, or 3/5 strength had mean glucose values of ∼169.8, 185.9, 177.3, and 172.8 mg/dL, respectively, whereas those with near-normal or full strength (4/5 or 5/5) had substantially lower mean glucose at 117.5 and 118 mg/dL.¹² In the third cohort, in the severe TSCI group, the mean admission glucose was 143.9 mg/dL ± 20.7 mg/dL, and the median glucose potassium ratio (GPR) was 2.21 ± 0.50.¹³ Across studies with explicit comparators, mean admission glucose was consistently around ∼150 mg/dL, while the normoglycemic were in the ∼105–110 mg/dL range. Pooled mean without weighting, these values correspond to ∼153 mg/dL in the hyperglycemic comprised of four cohorts,^10–14 versus ∼107 mg/dL in the normoglycemic group comprised of two cohorts.^10,11

Recovery

Admission hyperglycemia was also associated with poorer neurological and functional recovery by discharge. In one retrospective cohort, the frequency of an unfavorable AIS grade at follow-up increased at admission glucose thresholds of ≥ 126 mg/dL (OR 2.66, 95% CI: 1.52–4.72), ≥ 150 mg/dL (OR 2.62, 1.41–4.88), and ≥ 180 mg/dL (OR 3.70, 1.60–8.98).¹¹ Patients in the hyperglycemic group had lower American Spinal Injury Association (ASIA) motor scores, lower motor recovery rates, and Spinal Cord Independence Measurement (SCIM) scores at discharge, including smaller change in SCIM from admission to discharge (all p < 0.05).¹¹ Consistent with these findings, lack of AIS grade improvement was also more common among hyperglycemic patients (49 hyperglycemic patients with no AIS improvement vs. 30 normoglycemic patients), whereas large AIS improvements of two or three grades were more common in normoglycemic patients.¹¹ Length of acute hospitalization was prolonged in both groups but was numerically longer in patients with hyperglycemia (275.6 ± 18.6 days vs. 260.9 ± 20.2 days).¹¹ The mean duration of stress hyperglycemia was 2.7 ± 0.5 days.¹¹ In multivariate analysis higher admission glucose remained an independent predictor of worse motor outcomes.¹¹ In another retrospective study, admission glucose alone was associated with worse AIS outcomes, defined as grades A–C, on univariable analysis but lost significance after multivariable adjustment, whereas the GPR remained independently associated with poor 6-month AIS outcomes and demonstrated good discrimination (AUC 0.84, 95% CI: 0.808–0.875). The correlation with serum GPR and AIS grade over 6 months was moderate strength (R = −0.599, p < 0.001).¹⁴

Long-term neurological recovery showed a similar pattern when evaluated by chronic glycemic status. In a cohort stratified by HbA1c < 6.5% (well-controlled glycemia) versus HbA1c ≥ 6.5% (non–well-controlled), admission glucose differed between groups (∼109 mg/dL vs. 160 mg/dL), but initial AIS grades on admission did not differ meaningfully.¹¹ Despite comparable neurological status at presentation, the distribution of AIS improvement at 1 year differed significantly (p = 0.014).¹¹ Patients with HbA1c < 6.5% demonstrated more frequent two-grade and three-grade AIS improvements with 16 patients that improved by ≥ 2-grade, whereas patients with HbA1c ≥ 6.5% rarely achieved similar gains with 2 patients with a two-grade improvement and none with a three-grade improvement.¹¹ In univariable analysis, higher admission glucose was associated with poorer functional improvement (p = 0.007), but this relationship was no longer significant after multivariable adjustment (p = 0.186).¹¹ In contrast, elevated HbA1c (p = 0.015) remained an independent predictor of 1-year AIS improvement.¹¹ In a cross-sectional survey using the SF-12 found that hyperglycemia was independently associated with a worse HRQoL, particularly in physical function, 1 year after the injury. Specifically, hyperglycemia predicted a suboptimal Physical Component Summary (PCS < 50) with an OR of 2.57 (95% CI: 1.51–4.65). Univariate and multivariate analyses showed glucose to be significant in predicting PCS scores.¹⁵ Serial sampling in the NASCIS-3 cohort showed high early glycemia with decline by day 7 (time effect p < 0.0001). Hyperglycemia >140 mg/dL or >180 mg/dL at 24–48 hours was not associated with 1-year mortality (24 h: p = 0.8258 and 0.3662; 48 h: p = 0.8727 and 0.4113), whereas day 7 hyperglycemia at both thresholds predicted higher 1-year mortality (p < 0.0001 for each). In multivariable models adjusted for baseline neurological status and other covariates, hyperglycemia at 24 h, 48 h, or day 7 was not significantly associated with NASCIS motor, sensory, or pain scores at 6 weeks, 6 months, or 1 year. For disability, 24-hour hyperglycemia >140 mg/dL was independently associated with higher 1-year Functional Independence Measurement (FIM) (p = 0.0225) and showed a trend toward higher 6-month FIM (p = 0.0547), whereas day-7 hyperglycemia >140 mg/dL was associated with lower FIM at 6 weeks, 6 months, and 1 year (p < 0.05 for each). At the >180 mg/dL threshold, day-7 hyperglycemia showed only a trend toward lower FIM at 6 weeks (p = 0.0505), with no other significant adjusted associations with FIM.¹⁶

Discussion

We systematically mapped definitions and timing of early hyperglycemia in adults with acute TSCI against neurological and functional outcomes. The current evidence base is limited to retrospective cohorts and a serial dataset reanalysis with heterogeneous thresholds, sampling windows, and outcome instruments that preclude quantitative synthesis and restrict direct cross-study comparison. Across these studies, higher glucose in the acute period was generally associated with unfavorable AIS profiles and poorer functional recovery. Taken together, these findings support glucose as a candidate biomarker and potentially modifiable physiological domain in acute TSCI, while underscoring the absence of condition-specific glycemic targets or interventional trials.

Across the included studies, the relationship between early glycemia and outcome after acute TSCI appears time-dependent rather than uniformly linear. Glucose was most often measured at admission or at 24 hours, and findings in these early windows were inconsistent, with some cohorts reporting associations with worse neurological or functional status and others reporting null or attenuated effects after adjustment.^11–14,16 At day 7, Furlan (2021) reported that glucose categorized as >140 or >180 mg/dL was associated with higher 1-year mortality and lower FIM scores among survivors. In the same analysis, 24-h categories showed no statistically significant association with 1-year mortality or follow-up neurological scores.¹⁶

The inconsistency at admission is most plausibly explained by methodological and biological heterogeneity rather than by a uniform absence of effect. Exposure definitions differed, comparator groups were not standardized, and outcome instruments and windows varied, limiting cross-study coherence. Differences in case-mix and early care likely contributed as well: injury level and completeness, hemodynamics, sedation and analgesia, steroid exposure, timing of the first reliable neurological examination, and early infectious complications can influence both stress hyperglycemia and baseline scoring. On this background of heterogeneity, a consensus early glucose threshold for spinal cord injury is not evident.

When examining adjusted analyses across the available cohorts, a notable pattern emerges: the prognostic signal of early hyperglycemia is inconsistent once confounders are accounted for. Studies focused on neurological recovery using AIS grades generally report attenuation of significance after multivariable adjustment,^11,14 implying that admission glucose may reflect systemic stress or injury severity rather than exerting an independent effect. In contrast, two studies evaluating retained hyperglycemia as an independent predictor of worse motor score and PCS HRQoL,^11,15 suggesting that its influence may extend beyond neurological endpoints to broader functional domains. This divergence underscores the complexity of interpreting glycemic measures in SCI and highlights the need for future work to clarify whether glucose represents a modifiable risk factor or primarily a surrogate marker of physiological burden.

Alongside broader neurocritical literature, these studies might support treating dysglycemia as a clinically relevant prognostic factor. In TBI, randomized trials synthesized in a recent meta-analysis show that attempts at intensive control have not yielded consistent benefit and have increased hypoglycemia, a safety signal compounded by heterogeneous target ranges across trials, which complicates interpretation.⁴ Observational neuro–ICU data likewise indicate that early hyperglycemia tracks with worse outcomes after adjustment, reinforcing that abnormal glycemia is not benign.⁵ For SCI, the literature needs to standardize how glycemia is defined and reported and to test whether absolute glucose or composite measures provide independent, clinically meaningful prognostic information. If confirmed, the next question is a pragmatic one: identifying safe, operational ranges that minimize hypoglycemia while permitting clinicians to control for a measurable risk factor for poor neurological and functional outcomes in spinal cord injury.

The evidence on dysglycemia in acute TSCI is observational and heterogeneous in both exposure definitions and outcome windows. A single-center cohort assessed the admission GPR and its association with six-month AIS grade change; in that analysis, glucose alone was not predictive, whereas the composite showed prognostic value, which motivates evaluation of this marker in SCI and direct comparison with glucose in future work.¹⁷ Convergent findings across neurocritical populations further indicate that higher admission GPRs are repeatedly associated with adverse outcomes and, in several analyses, offer greater prognostic information than glucose alone.^17–26

Prospective studies should standardize biomarker ascertainment at admission, prespecify the calculation and units for the glucose-to-potassium ratio, and define preanalytic handling for potassium to minimize artifacts from hemolysis. To reduce confounding and improve interpretability, data collection should include steroid exposure, diabetes status with baseline HbA1c where feasible, and insulin protocols, with documentation of concomitant TBI when present. Outcomes should prioritize standardized neurological measures from the International Standards for Neurological Classification of Spinal Cord Injury, including AIS grade and AIS motor change, and incorporate patient-centered functional endpoints at 6–12 months, together with mortality. Future studies should combat the inconsistent exposure definitions, variable sampling schedules, and incomplete adjustment for key covariates. Multicenter designs, protocol preregistration, and transparent handling of missing data will enhance reproducibility and facilitate subsequent evidence synthesis. Collectively, these steps will determine whether the composite provides clinically meaningful prognostic information beyond glucose and whether its use is justified in future prognostic models for SCI.

Limitations

This review is subject to several limitations. First, all included studies were observational, predominantly retrospective cohorts, which introduces inherent risks of bias and limits causal inference. Second, there was substantial heterogeneity in both exposure definitions and outcome measures, making direct comparisons difficult. Third, the observational nature of the evidence precludes determination of whether hyperglycemia is a cause of worse outcomes or simply a marker of injury severity and systemic stress. Although some studies reported significant associations, these findings cannot establish causality. Fourth, while the review identifies signals that may warrant further investigation, it does not provide recommendations for glycemic management in TSCI. The evidence remains hypothesis-generating rather than practice-changing. Finally, limitations inherent to scoping reviews apply: the approach prioritizes breadth over depth, does not include formal risk-of-bias assessment, and does not synthesize effect sizes quantitatively, which restricts the ability to draw definitive conclusions about prognostic strength or clinical utility. These constraints underscore the need for standardized definitions, prospective designs, and rigorous adjustment strategies in future research.

Conclusion

The literature on hyperglycemia in acute TSCI is limited and heterogeneous, consisting mainly of observational studies that do not have consistent definitions of effect thresholds or justify clinical glycemic targets. Early hyperglycemia shows signals of association with poorer neurological and functional recovery, but definitions, sampling windows, and adjustment strategies remain inconsistent. Future work should prioritize multicenter prospective cohorts that use standardized measurement and outcome reporting to clarify prognostic value. Only after consistent associations and acceptable safety are demonstrated should randomized trials be considered to evaluate the impact on clinical outcomes.

Transparency, Rigor, and Reproducibility Summary

This scoping review was not formally registered, as protocol registration was not required. Overall, 2323 records were screened for inclusion. Six were found relevant to the study. Data collection and analysis were performed by investigators who were aware of the relevant characteristics of data. Data were collected in November 2025 using Preferred Reporting Items for Systematic Reviews and Meta-Analyses for scoping reviews. Data analysis took 1 month to complete. Methods that do not require correction for multiple comparisons were used, namely, systematic literature review. Key inclusion criteria are emerging standards in the field. No replication or external validation studies have been performed or are planned/ongoing at this time to our knowledge. Reproducibility will depend on database search terms and database selection. Analytic code is contained within the text. The authors received no financial support for the research, authorship, and/or publication of this article. The authors agree to provide the full content of the article on request by contacting Laura B. Ngwenya, MD, PhD.

Footnotes

Acknowledgments

The authors thank members of the University of Cincinnati College of Medicine Department of Neurosurgery for their support.

Authors’ Contributions

M.C.: Conceptualization, methodology, formal analysis, investigation, writing—original draft, and writing—review and editing. K.M.: Formal analysis, writing—original draft, and writing—review and editing. R.G.: Writing—original draft and writing—review and editing. C.C.: Writing—original draft and writing—review and editing. J.V.: Validation, writing—review and editing, and supervision. L.B.N.: Validation, writing—review and editing, and supervision.

Author Disclosure Statement

No competing financial interests exist.

Funding Information

No funding was received for this article.

Abbreviations Used

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