Abstract
Objective:
To investigate the relationship between blood alcohol concentration (BAC) and neurologic recovery after traumatic spinal cord injury (TSCI) using standardized outcome measures from the International Standards for the Neurological Classification of Spinal Cord Injury (ISNCSCI) examination.
Method:
This is a retrospective review of merged, prospectively collected, multicenter data from the Spinal Cord Injury Model Systems Database and institutional trauma databases from five academic medical centers across the United States. Patients with SCI and a documented BAC were analyzed for American Spinal Injury Association Impairment Scale (AIS) motor score, FIM, sensory light touch score, and sensory proprioception score upon admission and discharge from rehabilitation. Linear regression was used for the analysis.
Results:
The study identified 210 patients. Mean age at injury was 47 ± 20.5 years, 73% were male, 31% had an AIS grade A injury, 56% had ≥1 comorbidity, mean BAC was 0.42 ± 0.9 g/dL, and the mean Glasgow Coma Score upon arrival was 13.27 ± 4.0. ISNCSCI motor score gain positively correlated with higher BAC (4.80; confidence interval [CI], 2.39–7.22; p < .0001). FIM motor gain showed a trend toward correlation with higher BAC, although it did not reach statistical significance (3.27; CI, −0.07 to 6.61; p = .055). ISNCSCI sensory light touch score gain and sensory proprioception score gain showed no correlation with BAC (p = .44, p = .09, respectively).
Conclusion:
The study showed a positive association between higher BAC and neurologic recovery in patients with SCI as measured by ISNCSCI motor score gain during rehabilitation. This finding has not been previously reported in the literature and warrants further study to better understand possible protective physiological mechanisms underlying the relationship between BAC and SCI.
Keywords: alcohol, blood alcohol concentration, neuroprotection, outcomes, spinal cord injury
Introduction
The association between alcohol consumption and events leading to traumatic spinal cord injury (TSCI) is well established. Studies report alcohol consumption in about 21% to 47% of all SCI events.1–4 Alcohol and opioid use are the most frequent substances associated with SCI.5 In diving-related accidents that led to SCI, 15% to 49% were found to involve alcohol use, with one study demonstrating that subjects with higher blood alcohol concentration (BAC) were more likely to hit the bottom of the pool when diving and lacked insight into their increased risk of injury.6–9 Many patients continue to resume alcohol and substance abuse even after injury.10,11 Studies in a general trauma population have shown that alcohol consumption is associated with worse outcomes, although this finding is dependent on the injury type.12–14
Despite the prevalence of studies documenting the association between alcohol use and TSCI, few studies have investigated the influence of alcohol consumption on neurological outcomes in SCI. Research has shown an association between alcohol consumption and increased morbidity after SCI.3,4,15 However, studies regarding BAC and long-term neurological outcomes after SCI are scarce.
The study of alcohol consumption and SCI outcomes poses many challenges. Institutional trauma registries lack long-term outcome information beyond hospital discharge and typically do not measure variables and outcomes specific to SCI. Long-term outcome registries such as the multicenter SCI Model Systems (SCIMS) database lack many of the acute hospital variables, such as BAC, that can be used to study the association between alcohol consumption and neurological outcomes in SCI.
In this study, we examined data from the SCIMS-sponsored trauma registry merger module project to investigate how acute hospital BAC is associated with neurological outcomes for patients with SCI. Our hypothesis was that increased BAC would be associated with worse neurological outcomes as measured by International Standards for the Neurological Classification of Spinal Cord Injury (ISNCSCI) examination.
Material and Method
Data source
The SCIMS is a national project funded by the US Department of Health and Human Services, National Institute on Disability, Independent Living, and Rehabilitation Research (NIDILRR). The project is the first prospective, multicenter study of recovery and outcomes in patient with SCI following participation in a coordinated system of acute hospital care and SCI rehabilitation. Institutions that are designated as SCIMS centers must have access to level I trauma center care, acute spine surgery care, comprehensive inpatient rehabilitation services, and long-term interdisciplinary follow-up and rehabilitation services. Currently there are 14 SCIMS centers and five additional follow-up centers across the United States. SCIMS database inclusion criteria are (1) TSCI that is associated with a motor or sensory deficit, (2) admission to an SCIMS center within 1 year of injury, (3) acute hospital care and inpatient rehabilitation received within a participating SCIMS center, and (4) informed consent signed by the patient and/or guardian. More information is available at: https://www.nscisc.uab.edu/nscisc-database.aspx.
Data for this project were generated by merging patient data from SCIMS databases with acute hospital trauma registries from five separate trauma regions across the United States. All participating SCIMS centers in this project were also designated level I trauma centers by the American College of Surgeons (https://www.facs.org/search/trauma-centers). Level I trauma centers provide data on all traumatic injuries for inclusion into the National Trauma Bank (https://www.facs.org/quality-programs/trauma/tqp/center-programs/ntdb/about). The data collected for the trauma module reflect the data collected for the NTDB by each center’s hospital trauma registry team.
A deterministic matching method for merging each center’s trauma data (TD) with their corresponding SCIMS data was employed. Each participating SCIMS center acquired all TD for SCI patients between October 2016 through December 2018, with one SCIMS center providing an additional 49 cases for the SCIMS period of 2010–2011. Each participating SCIMS center organized the data into a new shared database that merged patient data from the trauma registry with patient data in the SCIMS database. At each center, the data manager assigned the patient’s corresponding SCIMS patient ID and system ID as the identifiers for matching and then merged each patient’s SCIMS data with each patient’s trauma registry data. This new merged database was then uploaded by each SCIMS center to a new database at the SCIMS National Statistical Center. The combined database from all participating centers was then downloaded to the lead SCIMS center. The lead center made the combined trauma database available to the SCIMS participating centers. Data use agreements with the lead center were completed prior to sending out the combined trauma database.
Patient selection and characteristics
We analyzed all acute hospital trauma variables known to influence postdischarge outcomes in SCI patients that were available in the merged SCIMS database. Race was dichotomized into African American and non–African American; ethnicity is available in the SCIMS database but was not reported in this study. Medical comorbidities were defined as any of the following disorders present on admission: hypertension, smoking, diabetes, bleeding disoders, cancer, heart disease, renal failure, cerebrovascular accident, chronic obstructive pulmonary disease (COPD), cirrhosis, dementia, anticoagulant use, myocardial infaraction, peripheral artery disease, and substance abuse. BAC is defined in grams per deciliter (g/dL) and was obtained within 24 hours of the first hospital encounter, typically upon initial evaluation of the patient in the emergency department.16 The neurological level of injury (NLOI) was measured according to the ISNCSCI, and completeness of injury was documented using the American Spinal Injury Association Impairment Scale (AIS). The NLOI was recoded into groups as “cervical” for C1–C8 injuries, “thoracic” for T1–T11 injuries, and “lumbar” for T12-L5 injuries for clinical descriptive purposes. Only the raw NLOI score was used to calculate changes in the NLOI over time. Penetrating injury was defined as any gunshot wound, knife wound, explosion, and any other penetrating type wound.
Outcomes
Outcomes were measured at SCI rehabiliation admission and discharge including the AIS, the AIS motor and sensory scores, FIM motor scores, and NLOI scores. Patients with complete SCIs as measured by the AIS were coded AIS A and were analyzed separately from patients with incomplete SCIs coded AIS B through D based upon known differences in neurological outcomes between these two groups.17,18 Changes in AIS grade over time were measured by recoding each AIS alpha score into a numerical score and subtracting the AIS numerical score at SCI rehabilitation discharge from the initial AIS score obtained at SCI rehabilitation admission. Changes in NLOI over time were measured by recoding each neurological level of injury grade into a numerical score and subtracting the numerical score at SCI rehabilitation discharge from the initial numerical score obtained at SCI rehabilitation admission.
Statistical analyses
Multivariate, non-stepwise linear regression analysis was performed to determine independent predictors of AIS motor gain, FIM motor gain, sensory light touch gain, and sensory proprioception gain from SCI rehabilitation admission to discharge. Analyses were performed using SPSS software (version 25.0; SPSS, Inc., Chicago, IL). Statistical significance was set at p < .05.
Results
A total of 210 SCI patients were merged across trauma registries and the SCIMS databases. Average age of the SCI population was 47 ± 18.9 years, and most patients were male. Patients with complete injuries (i.e., AIS A) were about 31% of the study population. The average AIS motor gain from rehabilitation admission to discharge was 10.5 ± 12.6, and average score gains for FIM motor, sensory light touch, and sensory proprioception were 28.2 ± 17.1, 8.4 ± 18.5, and 8.3 ± 19.8, respectively. A majority of patients presented with more than one medical comorbidity. Average BAC on admission to the acute hospital was 0.42 g/dL. Average injury severity score (ISS) in this population was 22, and most of the patients were admitted with cervical SCIs (Table 1).
Table 1.
Baseline admission characteristics for merged SCI trauma patient data (N = 210)
| Characteristic | Mean ± SD or n (%) |
|---|---|
| Age, years | 47 ± 18.9 |
| Male | 153 (73%) |
| AIS scorea | |
| A | 64 (31%) |
| B | 15 (7%) |
| C | 38 (18%) |
| D | 73 (35%) |
| AIS motor gain | 10.5 ± 12.6 |
| FIM motor gain | 28.2 ± 17.1 |
| Sensory light touch gain | 8.4 ± 18.5 |
| Sensory proprioception gain | 8.3 ± 19.8 |
| Total comorbidities | |
| ≥1 | 117 (56%) |
| Smoker | 52 (25%) |
| HTN | 50 (24%) |
| BAC, % | 0.42 ± 0.86 |
| ISS | 22 ± 11.9 |
| NLOI | |
| Cervical | 124 (59%) |
| Thoracic | 56 (27%) |
| Lumbosacral | 8 (4%) |
Note: All continuous variables are reported at average values with standard deviations. AIS = American Spinal Injury Association Impairment Scale; BAC = blood alcohol concentration; HTN = hypertension; ISS = injury severity score; NLOI = neurological level of injury; SCI = spinal cord injury.
Statistically significant.
Does not total 100% due to missing scores.
Linear regression analysis showed that higher BAC at acute hospital admission was an independent predictor of AIS motor gain from rehabilitation admission to discharge (beta coefficient = 4.80; confidence interval [CI], 2.39–7.22; R2 = 0.29). The presence of an incomplete SCI was also an independent predictor of AIS motor gain at discharge from rehabilitation (beta coefficient = 8.25; CI, 3.25–13.24; R2 = 0.29). Total comorbidities, age at injury, ISS, and the NLOI showed no association with AIS motor gain (Table 2).
Table 2.
Linear regression for AIS motor gain
| 95% CI for beta | |||||
|---|---|---|---|---|---|
| Model | Beta | SE | p | Lower | Upper |
| Age at injury, years | 0.05 | 0.06 | .45 | −0.08 | 0.17 |
| Male | 4.59 | 2.42 | .06 | −0.20 | 9.38 |
| African American | 1.07 | 2.45 | .66 | −3.79 | 5.92 |
| Total comorbidities | 0.27 | 0.72 | .70 | −1.14 | 1.69 |
| BAC | 4.80 | 1.22 | <.0001* | 2.39 | 7.22 |
| GCS | 0.05 | 0.29 | .86 | −0.53 | 0.63 |
| ISS | −0.06 | 0.10 | .57 | −0.27 | 0.15 |
| Incomplete SCI | 8.25 | 2.52 | .001* | 3.25 | 13.24 |
| NLOI | −0.24 | 0.17 | .16 | −0.58 | 0.09 |
| R2 = 0.29 | |||||
Note: BAC and GCS were obtained in the emergency department. AIS = American Spinal Injury Association; BAC = blood alcohol level; CI = confidence interval; GCS = Glasgow Coma Score; ISS = injury severity score; NLOI = neurological level of injury; SCI = spinal cord injury.
Statistically significant.
Linear regression analysis did not demonstrate a statistically significant association between BAC and FIM motor gain, sensory light touch gain, and sensory proprioception gain. However, higher BAC did show a trend toward significance in FIM motor gain (beta coefficient = 3.27; CI, −0.07 to 6.61; R2 = 0.23). A lower NLOI was also associated with FIM motor gain in this model (beta coefficient = 0.56; CI, 0.09–1.03; R2 = 0.23) (Table 3). No clinically relevant injury characteristics were associated with score gains in sensory light touch and sensory proprioception from rehabilitation admission to discharge (Tables 4 and 5).
Table 3.
Linear regression for FIM motor gain
| 95% CI for beta | |||||
|---|---|---|---|---|---|
| Model | Beta | SE | p | Lower | Upper |
| Age at injury, years |
−0.05 | 0.09 | .56 | −0.22 | 0.12 |
| Male | −2.53 | 3.35 | .45 | −9.16 | 4.10 |
| African American | 3.79 | 3.40 | .27 | −2.93 | 10.52 |
| Total comorbidities | −1.06 | 0.99 | .29 | −3.02 | 0.90 |
| BAC | 3.27 | 1.69 | .06 | −0.07 | 6.61 |
| GCS | 0.42 | 0.41 | .30 | −0.38 | 1.22 |
| ISS | −0.06 | 0.14 | .68 | −0.34 | 0.22 |
| Incomplete SCI | 13.54 | 3.50 | <.0001* | 6.63 | 20.45 |
| NLOI | 0.56 | 0.24 | .02* | 0.09 | 1.03 |
| R2 = 0.23 | |||||
Note: BAC and GCS were obtained in the emergency department. BAC = blood alcohol level; CI = confidence interval; GCS = Glasgow Coma Score; ISS = injury severity score; NLOI = neurological level of injury; SCI = spinal cord injury.
Statistically significant.
Table 4.
Linear regression for sensory light touch gain
| 95% CI for beta | |||||
|---|---|---|---|---|---|
| Model | Beta | SE | p | Lower | Upper |
| Age at injury, years |
0.04 | 0.12 | .72 | −0.20 | 0.29 |
| Male | 11.68 | 4.82 | .02* | 2.10 | 21.28 |
| African American | −6.05 | 4.89 | .22 | −15.78 | 3.70 |
| Total comorbidities | −0.32 | 1.42 | .82 | −3.15 | 2.52 |
| BAC | 1.87 | 2.43 | .44 | −2.96 | 6.71 |
| GCS | 0.09 | 0.58 | .88 | −1.07 | 1.25 |
| ISS | 0.11 | 0.21 | .60 | −0.30 | 0.52 |
| Incomplete SCI | 0.85 | 5.02 | .87 | −9.16 | 10.86 |
| NLOI | −0.45 | 0.34 | .19 | −1.13 | 0.23 |
| R2 = 0.12 | |||||
Note: BAC and GCS were obtained in the emergency department. BAC = blood alcohol level; CI = confidence interval; GCS = Glasgow Comas Score; ISS = injury severity score; NLOI = neurological level of injury; SCI = spinal cord injury.
Statistically significant.
Table 5.
Linear regression for sensory proprioception gain
| 95% CI for beta | |||||
|---|---|---|---|---|---|
| Model | Beta | SE | p | Lower | Upper |
| Age at injury, years |
0.14 | 0.13 | .30 | −0.12 | 0.40 |
| Male | 7.23 | 5.10 | .16 | −2.88 | 17.34 |
| African American | −8.13 | 5.15 | .12 | −18.40 | 2.12 |
| Total comorbidities | −0.30 | 1.50 | .84 | −3.29 | 2.69 |
| BAC | 4.35 | 2.56 | .09 | −0.75 | 9.44 |
| GCS | 0.04 | 0.61 | .95 | −1.18 | 1.26 |
| ISS | 0.17 | 0.22 | .45 | −0.27 | 0.60 |
| Incomplete SCI | 3.56 | 5.30 | .50 | −6.99 | 14.10 |
| NLOI | −0.44 | 0.36 | .22 | −1.16 | 0.27 |
| R2 = 0.14 | |||||
Note: BAC and GCS were obtained in the emergency department. BAC = blood alcohol level; CI = confidence interval; GCS = Glasgow Comas Score; ISS = injury severity score; NLOI = neurological level of injury; SCI = spinal cord injury.
Discussion
Our study shows that higher BAC at acute hospital admission is an independent predictor of increased AIS motor score improvement at discharge from SCI rehabilitation. A similar trend toward significance was observed in the association between BAC and FIM motor gain. These models also demonstrate that incomplete SCI and a lower level of SCI is associated with greater improvement in AIS and FIM motor gains at discharge from rehabilitation and that no association was observed between BAC and sensory score improvements.
To our knowledge, this is the first study to demonstrate an association between BAC and neurological outcomes for patient with SCI. A paper published in 2013 by Furlan and Fehlings analyzed data from the NASCIS-3 study and found no association between BAC and functional outcomes defined as FIM motor improvement at 6 weeks, 6 months, and 1 year post SCI.15 The Furlan and Fehlings paper was a secondary analysis of the NASCIS-3 trial data, which was a prospective, randomized trial published in 1997 and designed to assess the effect of high-dose steroid administration on neurological recovery after SCI. High-dose steroids are rarely used in the current management of acute SCI, so these findings may not have application today. Moreover, in our study we observed a trend toward significance in the relationship between BAC and FIM motor gain. Our findings suggest that AIS motor gain may be a more sensitive outcome measure for functional improvement in this population.
Animal studies of BAC and SCI are scarce. Rodent-based studies suggest no association between BAC and functional outcomes after SCI although in vitro work does suggest neuronal toxicity associated with high alcohol concentrations.19,20 Clinical outcomes studies in traumatic brain injury (TBI) suggest that higher BAC may have a beneficial effect on survival and functional outcomes in TBI,21–25 although some of these findings may be attributed to residual confounding of non-measured injury-related factors.26
Our study corroborates these previous clinical TBI studies that suggest that BAC may play a potentially protective role in neurological recovery after injury. The biological basis for the possible protective role of alcohol and neurological injury has been studied. Early studies of N-methyl-D-aspartate antagonists (NMDA) suggested a neuroprotective role for alcohol in TBI by limiting receptor mediated excitotoxicity.27 However, subsequent large-scale clinical trials demonstrated no benefit in these agents for patients with TBI likely due to dynamic changes in NMDA receptor functionality after injury.28 Additional mechanisms such as alcohol-mediated reduction in catecholamine surge after injury has also been studied in TBI and suggests a protective effect from alcohol in neurological injury.29,30 Most research on the effects of alcohol and neurological injury has focused on TBI, and very few studies have examined SCI specifically. Improved SCI motor recovery in patients with higher BAC may be due to the neuroprotective effects of alcohol, although further study is needed to elucidate any specific neuroprotective mechanisms in SCI.
Limitations
This study was a retrospective analysis of prospectively collected data and carries several biases related to retrospective analysis including selection bias. Clinical studies in SCI are typically limited by population heterogeneity and lack multiple standardized outcome measures. We stratified the injury severity of our study population in order to analyze a more homogenous population and analyze their outcomes across several standardized outcomes measures and scores. However, the results of this study might not apply to patients with SCI who are not admitted to SCI rehabilitation at acute care hospital discharge or who are not treated in a SCIMS institution. Finally, about 30% of sensory light touch and sensory proprioception scores were missing at discharge from rehabilitation, which limited the power of the linear regression models to detect associations among predictor variables and sensory score outcomes.
Conclusion
Increased BAC at hospital admission is associated with greater AIS motor gain at discharge from SCI rehabilitation using the SCIMS multicenter merged trauma database. Further research is needed to determine the relationship between increased BAC and a protective advantage for patients with acute SCI.
Footnotes
Financial Support
The SCI Model Systems national database is a multicenter study of the SCI Model System Centers Program and is supported by the National Institute on Disability, Independent Living and Rehabilitation Research (NIDILRR), a center within the Administration for Community Living (ACL), Department of Health and Human Services (HHS). However, these contents do not necessarily reflect the opinions or views of the SCI Model System Centers, NIDILRR, ACL, or HHS.
Conflicts of Interest
The authors report no conflicts of interest.
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