Sage Journals: Discover world-class research

Abstract

Study Design

A retrospective database analysis.

Objective

To determine the incidence of lower extremity deep vein thrombosis (DVT) and identify risk factors associated with DVT development in patients with spinal cord injury (SCI), stratified by level of injury.

Methods

The National Inpatient Sample from 2016 to 2021 was used to identify adult inpatients with SCI who developed DVT within the same admission and to categorize them by anatomical injury level. Multivariable logistic regression was used to assess independent risk factors by SCI level.

Results

Among 59,498 SCI patients, the overall DVT incidence was 2.8%. The DVT rate was lowest in cervical SCI (2.6%) and highest in thoracic SCI (3.2%). Pulmonary embolism was a strong independent risk factor for DVT across all SCI levels ([Cervical] OR: 12.82, CI: 10.46-15.63, [Thoracic] OR: 11.82, CI: 9.13-15.20, [Lumbar] OR: 11.38, CI: 6.74-18.74). For cervical SCI, risk factors included coagulopathies (OR: 1.90, CI: 1.54-2.32), older age (OR: 1.01, CI: 1.01-1.02), complete (OR: 1.84, CI: 1.43-2.35) or incomplete cervical lesion (OR: 1.38, CI: 1.17-1.63), cervical (OR: 1.34, CI: 1.16-1.54) or lumbar fracture (OR: 1.58, CI: 1.17-2.11), and upper extremity DVT (OR: 3.58, CI: 2.53-4.97). For thoracic SCI, risk factors included thoracic fracture (OR: 1.46, CI: 1.20-1.77), upper extremity DVT (OR: 3.82, CI: 2.18-6.36), and fluid/electrolyte disorder (OR: 1.35, CI: 1.13-1.62). For lumbar SCI, fluid/electrolyte disorder (OR: 1.92, CI: 1.38-2.66) was an independent predictor.

Conclusion

DVT incidence and risk factors vary by SCI level. Identifying these factors is critical for stratifying care and developing tailored prophylactic strategies that prevent adverse events and optimize patient outcomes.

Keywords

trauma spinal cord injury cervical thoracic lumbar deep vein thrombosis risk factors NIS

Background

Traumatic spinal cord injury (SCI) results from an acute insult to the spinal cord, leading to transient or permanent neurologic deficits below the level of injury.^1,2 In the United States, SCI has an annual incidence of roughly 54 per million, translating to approximately 18,000 new cases yearly.³ Patients with SCI are susceptible to a range of complications that significantly decrease life expectancy,^1,2,4 among which thromboembolic events represent a major concern. Among all hospitalized trauma patients, those with SCI have the highest risk for deep vein thrombosis (DVT) development,⁵ with earlier studies reporting DVT rates as high as 100% in the absence of prophylaxis.^6,7

Despite advancements in prophylactic management, DVT and its most serious complication, pulmonary embolism (PE), remain one of the leading causes of mortality in this population.^8,9 Notably, long-term survival outcomes for patients with SCI have shown minimal improvement over the past several decades.^4,10,11 DVT originating in the lower extremities poses a particularly high risk for progression to clinically significant PE,^12,13 with the greatest mortality risk from thromboembolism occurring within the first three months post-injury.^14-20

Previous studies have proposed various potential risk factors for DVT development in SCI, including older age, race, male sex, comorbidities, and paraplegia.^{5,16,18,21-24} However, these findings have been largely inconclusive due to small sample sizes and limited generalizability of single-institution studies.^{5,16,18,22,24} More crucially, prior studies have examined risk factors for DVT across all spinal levels in SCI, yet emerging evidence suggests that thromboembolic risk and complications vary substantially depending on the level of injury.^17,25-27 Large-scale, multicenter studies utilizing nationally representative population data remain scarce, and no study to date has thoroughly investigated the DVT risk factors in relation to the different SCI levels. The present study aims to fill this critical gap by leveraging data from the National Inpatient Sample (NIS) database to stratify risk factors for lower extremity DVT by SCI level. To our knowledge, this is the first study to identify demographic and clinical risk factors associated with the development of symptomatic lower extremity DVT by level of SCI using a large population database.

Materials and Methods

Study Design and Setting

This is a retrospective study analyzing the de-identified patient data set from the National Inpatient Sample (NIS). The NIS is one of the largest publicly available databases of inpatient healthcare information in the United States (US). It captures approximately 98% of the US patient population across roughly 4500 hospitals in 49 states participating in the Healthcare Cost and Utilization Project (HCUP), sponsored by the Agency for Healthcare Research and Quality (AHRQ).²⁸ NIS is a 20% stratified sample of all discharges from US community hospitals, including specialty hospitals, public hospitals, academic medical centers, and long-term acute care facilities.²⁹ Annually, the NIS data reports on over 7 million hospital stays, providing detailed discharge information such as International Classification of Diseases (ICD) codes, demographics, comorbidity measures, and other variables.²⁸ Data collection and management is a collaboration between experienced community hospital staff, medical administrators of state and private organizations, hospital associations, and the federal government.^28,30 The HCUP and AHRQ are not responsible for the conclusions drawn from this analysis. Due to the implementation of ICD-10-CM in October 2015, the analysis was restricted to data collected after 2015.³¹

Eligibility Criteria

The 2016 to 2021 NIS database was used to identify adult (>18 years old) inpatients with a primary diagnosis of cervical SCI, thoracic SCI, and lumbar SCI. All patients with non-traumatic SCI were excluded. Among the SCI cohort, patients who developed DVT were selected for the final analysis.

Variables

The records were segregated into different spinal levels and compared between those who developed DVT vs those who did not. Data were collected on two main domains, namely:

(a) Demographic characteristics: Age, sex, race, insurance status, patient location, etc.

(b) Clinical data: Length of stay, costs, smoking status, Elixhauser comorbidity index (ECI),³² and mortality.

Neurological injury was categorized into complete and incomplete spinal cord lesions. A complete SCI was defined as the total absence of sensory and motor function in the lowest sacral segments S4-5.³³ An incomplete SCI was defined as the preservation of any sensory or motor function below the neurological level that includes the lowest sacral segments S4-5.³⁴ The ECI paralysis variable was excluded to avoid redundancy with the SCI classification.

Data Management and Missing Data

Data was extracted using password-protected Microsoft ® Excel for Microsoft 365, version 2206 - Build 15330.20306 (Publisher: Microsoft Corporation, Redmond, Washington, USA, 2022). The de-identified patient data were analyzed using the Statistical Analysis System for Windows, Version 9.4 (Publisher: SAS Institute Inc., Cary, North Carolina, USA, 2013). The pairwise deletion method was utilized to deal with variables with missing data points.

Quantitative Variables and Statistical Methods

Demographic characteristics and clinical data, including history of infections, medical history, and laboratory data, were summarized using descriptive statistics. All monetary values were reported in United States Dollar (USD). The normal distribution of data was verified using Kolmogorov-Smirnov’s normality test. Continuous variables were represented as Mean (Standard Deviation - SD), and categorical variables as frequency (percentage). Categorical variables with normal distribution were compared using Pearson’s Chi-square statistical tests. Between-group comparisons (DVT versus no DVT) were made using z-test with P-values adjusted using the Bonferroni method. After the univariate analysis, multivariable logistic regression was done, adjusting for age, sex, race, and selected comorbidities to characterize statistical associations with the development of DVT. Statistical significance for all analyses was set at P < 0.05.

Results

Incidence

Among 59,498 patients with SCI between 2016 and 2021, the overall incidence of DVT was 2.8% (n = 1674). Stratification by anatomical injury level showed that patients with cervical SCI had the lowest DVT rate (2.6%, P < 0.001), while those with thoracic SCI had the highest (3.2%, P < 0.01). Overall, SCI at any level was significantly associated with DVT development (P < 0.001) (Table 1).

Table 1.

Incidence Rates of Deep Vein Thrombosis by Spinal Cord Injury Levels

Anatomical Location of SCI	Total # of patients (N(%))	DVT (N(%))	No DVT (N(%))	DVT rate (%)	P-value^a
Cervical	36846 (61.9)	956 (57.1)	35890 (62.1)	2.6	<0.001
Thoracic	17319 (29.1)	554 (33.1)	16765 (29.0)	3.2	<0.001
Lumbar	5333 (9.0)	164 (10.0)	5169 (8.9)	3.1	>0.05
Total	59498 (100)	1674 (100)	57824 (100)	2.8	--

Overall chi-squared analysis demonstrates an association between SCI level and DVT incidence across all spinal levels analyzed (χ2 = 17.20, df = 2, P = 0.00018).

DVT: Deep Vein Thrombosis.

SCI: Spinal Cord Injury.

Bolded values indicate statistical significance.

^aComparisons were conducted using the chi-squared test.

Patient Demographics and Characteristics

Among the 36,846 patients with cervical SCI, 2.6% (n = 956) developed a DVT. Patients with lower extremity DVT were older (57.2 ± 16.9 vs 55.4 ± 18.8 years, P < 0.001) and more likely to have concomitant thrombotic complications, including pulmonary embolism (17.4% vs 1.3%, P < 0.001) and upper extremity DVT (5.3% vs 0.9%, P < 0.001) compared to those without DVT (Table 2). Comorbidities, including diabetes mellitus, hypertension, and obesity, were not associated with DVT risk. The details of additional comorbidities are summarized in Supplemental Table 1A.

Table 2.

Demographic Characteristics of Patients With Cervical Spinal Cord Injury With or Without Lower Extremity Deep Vein Thrombosis Between 2016 and 2021 in the United States

Category	Total # of patients with cervical SCI (N(%))	Cervical SCI and LE DVT (N(%))	Cervical SCI and no LE DVT (N(%))	P value^a
Number of admissions (N(%))	36846 (100)	956 (2.6)	35890 (97.4)	--
Mean age (yr)	55.5±18.7	57.2±16.9	55.4±18.8	<0.001
Sex (N(%))
Male	27474 (74.6)	774 (81.0)	26700 (74.4)	>0.05
Female	9366 (25.4)	182 (19.0)	9184 (25.6)	>0.05
N/A	6 (0.0)	0	6 (0.0)	>0.05
Race (N(%))
White	22391 (60.8)	559 (58.5)	21832 (60.8)	>0.05
Black	7572 (20.6)	227 (23.7)	7345 (20.5)	>0.05
Hispanic	3137 (8.5)	63 (6.6)	3074 (8.6)	>0.05
Asian or Pacific Islander	978 (2.7)	23 (2.4)	955 (2.7)	>0.05
Native American	323 (0.9)	5 (0.5)	318 (0.9)	>0.05
Other	1045 (2.8)	30 (3.1)	1015 (2.8)	>0.05
N/A	1400 (3.8)	49 (5.1)	1351 (3.8)	>0.05
Mean length of stay (days)	11.6±16. 2	21.5±23.6	11.4±15.9	<0.001
Mean total charge (USD)	$164,086.2+$256,539.1	$305,871.2±$379,281.4	$160,346.3±$251,422.9	<0.001
Mean until first procedure (days)	2.4±5.8	3.5±6.7	2.4±5.7	<0.001
Mortality (N(%))
Died	2074 (5.6)	75 (7.8)	1999 (5.6)	<0.001
Did not die	34741 (94.3)	881 (92.2)	33860 (94.3)	<0.05
Primary insurance (N(%))
Medicare	16484 (44.7)	370 (38.7)	16114 (44.9)	<0.01
Medicaid	7410 (20.1)	197 (20.6)	7213 (20.1)	>0.05
Private insurance	9259 (25.1)	303 (31.7)	8956 (25.0)	>0.05
Self-pay	1452 (3.9)	19 (2.0)	1433 (4.0)	<0.05
No charge	108 (0.3)	4 (0.4)	104 (0.3)	>0.05
Other	2063 (5.6)	61 (6.4)	2002 (5.6)	>0.05
N/A	70 (0.2)	2 (0.2)	68 (0.2)	>0.05
Smoking status
Yes	4888 (13.3)	94 (9.8)	4794 (13.4)	<0.001
No	31958 (86.7)	862 (90.2)	31096 (86.6)	<0.001
Concomitant injuries
Pulmonary embolism	623 (1.7)	166 (17.4)	457 (1.3)	<0.001
Upper extremity deep vein thrombosis	386 (1.0)	51 (5.3)	335 (0.9)	<0.001
Fracture of cervical spine	11862 (32.2)	415 (43.4)	11447 (31.9)	<0.001
Fracture of thoracic spine	2708 (7.3)	116 (12.1)	2592 (7.2)	<0.001
Fracture of lumbar spine	1133 (3.1)	61 (6.4)	1072 (3.0)	<0.001
Complete lesion of cervical spinal cord	1662 (4.5)	91 (9.5)	1571 (4.4)	<0.001
Complete lesion of thoracic spinal cord	59 (0.2)	3 (0.3)	56 (0.2)	>0.05
Complete lesion of lumbar spinal cord	2 (0.0)	0	2 (0.0)	>0.05
Incomplete lesion of cervical spinal cord	6214 (16.9)	220 (23.0)	5994 (16.7)	<0.001
Incomplete lesion of thoracic spinal cord	166 (0.5)	11 (1.2)	155 (0.4)	<0.01
Incomplete lesion of lumbar spinal cord	6 (0.0)	0	6 (0.0)	>0.05
Atrial fibrillation	3778 (10.3)	109 (11.4)	3669 (10.2)	>0.05
Cervical spinal cord injury	36846 (100)	956 (100)	35890 (100)	NA
Thoracic spinal cord injury	676 (1.8)	30 (3.1)	646 (1.8)	>0.05
Lumbar spinal cord injury	89 (0.2)	4 (0.4)	85 (0.2)	>0.05
Comorbidities
Acquired immune deficiency syndrome (AIDS)	835 (2.3)	40 (4.2)	795 (2.2)	<0.05
Coagulopathy	2365 (6.4)	128 (13.4)	2237 (6.2)	<0.001
Depression	5673 (15.4)	99 (10.4)	5574 (15.5)	<0.001
Fluid and electrolyte disorder	12625 (34.3)	405 (42.4)	12220 (34.0)	<0.001
Pulmonary circulatory disorder	1097 (3.0)	171 (17.9)	926 (2.6)	<0.001
Weight loss	3742 (10.2)	131 (13.7)	3611 (10.1)	<0.05

N/A: missing data.

LE DVT: Lower Extremity Deep Vein Thrombosis.

SCI: Spinal Cord Injury.

USD: United States Dollar.

Bolded values indicate statistical significance.

^aComparisons were conducted using the z-test with P-values adjusted using the Bonferroni method.

Among the 17,319 patients with thoracic SCI cohort, 3.2% (n = 554) developed a DVT. Those with lower extremity DVT were older (48.6 ± 18.5 vs 47.1 ± 19.2 years, P < 0.001) and more frequently had concurrent conditions such as pulmonary embolism (18.6% vs 1.6%, P < 0.001), upper extremity DVT (3.6% vs 0.7%, P < 0.001), fluid and electrolyte disorders (43.7% vs 33.6%, P < 0.001), and pulmonary circulatory disorder, defined as conditions affecting blood flow through the lungs, such as, pulmonary hypertension (19.9% vs 2.8%, P < 0.001) (Table 3). As with cervical SCI, comorbidities were not significantly associated with DVT risk. The details of additional comorbidities are summarized in Supplemental Table 1B.

Table 3.

Demographic Characteristics of Patients With Thoracic Spinal Cord Injury With or Without Lower Extremity Deep Vein Thrombosis Between 2016 and 2021 in the United States

Category	Total # of patients with thoracic SCI (N(%))	Thoracic SCI and LE DVT (N(%))	Thoracic SCI and no LE DVT (N(%))	P value^a
Number of admissions (N(%))	17319 (100)	554 (3.2)	16765 (96.8)	--
Mean age (yr)	47.2±19.1	48.6±18.5	47.1±19.2	<0.001
Sex (N(%))
Male	12945 (74.7)	440 (79.4)	12505 (74.6)	<0.05
Female	4368 (25.2)	114 (20.6)	4254 (25.4)	<0.05
N/A	6 (0.0)	0	6 (0.0)	>0.05
Race (N(%))
White	9784 (56.5)	326 (58.8)	9458 (56.4)	>0.05
Black	3893 (22.5)	120 (21.7)	3773 (22.5)	>0.05
Hispanic	2016 (11.6)	54 (9.7)	1962 (11.7)	>0.05
Asian or Pacific Islander	292 (1.7)	6 (1.1)	286 (1.7)	>0.05
Native American	223 (1.3)	5 (0.9)	218 (1.3)	>0.05
Other	488 (2.8)	26 (4.7)	462 (2.8)	>0.05
N/A	623 (3.6)	17 (3.1)	606 (3.6)	>0.05
Mean length of stay (days)	11.9±15.1	21.3±23.2	11.6±14.7	<0.001
Mean total charge (USD)	$156,243.1±$257,568.8	$322,561.9±$449,922.5	$150,822.6±$246,956.2	<0.001
Mean until first procedure (days)	2.5±5.4	3.8±7.4	2.4±5.3	<0.001
Mortality (N(%))
Died	448 (2.6)	18 (3.2)	430 (2.6)	>0.05
Did not die	16858 (97.3)	536 (96.8)	16322 (97.4)	>0.05
N/A	13 (0.0)	0	13 (0.0)	>0.05
Primary insurance (N(%))
Medicare	6614 (38.7)	186 (33.6)	6428 (38.3)	>0.05
Medicaid	4974 (28.7)	140 (25.2)	4834 (28.8)	>0.05
Private insurance	4076 (23.5)	163 (29.4)	3913 (23.3)	<0.01
Self-pay	623 (3.6)	23 (4.2)	600 (3.6)	>0.05
No charge	37 (0.2)	1 (0.2)	36 (0.2)	>0.05
Other	972 (5.6)	40 (7.2)	932 (5.6)	>0.05
N/A	23 (0.1)	1 (0.2)	22 (0.1)	>0.05
Smoking status
Yes	2789 (16.1)	64 (11.6)	2725 (16.3)	<0.01
No	14530 (83.9)	490 (88.4)	14040 (83.7)	<0.01
Concomitant injuries
Pulmonary embolism	367 (2.1)	103 (18.6)	264 (1.6)	<0.001
Upper extremity deep vein thrombosis	135 (0.8)	20 (3.6)	115 (0.7)	<0.001
Fracture of cervical spine	1141 (6.6)	62 (11.2)	1079 (6.4)	<0.001
Fracture of thoracic spine	5538 (32.0)	257 (46.4)	5281 (31.5)	<0.001
Fracture of lumbar spine	1551 (8.9)	78 (14.1)	1473 (8.8)	<0.001
Complete lesion of cervical spinal cord	44 (0.3)	5 (0.9)	39 (0.2)	<0.05
Complete lesion of thoracic spinal cord	2003 (11.6)	103 (18.6)	1900 (11.3)	<0.001
Complete lesion of lumbar spinal cord	20 (0.1)	0	20 (0.1)	>0.05
Incomplete lesion of cervical spinal cord	162 (0.9)	9 (1.6)	153 (0.9)	>0.05
Incomplete lesion of thoracic spinal cord	2868 (16.6)	134 (24.2)	2734 (16.3)	<0.001
Incomplete lesion of lumbar spinal cord	61 (0.4)	5 (0.9)	56 (0.3)	>0.05
Atrial fibrillation	1151 (6.6)	40 (7.2)	1111 (6.6)	>0.05
Cervical spinal cord injury	675 (3.9)	31 (5.6)	644 (3.8)	>0.05
Thoracic spinal cord injury	17319 (100)	554 (100)	16765 (100)	NA
Lumbar spinal cord injury	477 (2.8)	20 (3.6)	457 (2.7)	>0.05
Comorbidities
Acquired immune deficiency syndrome (AIDS)	359 (2.1)	18 (3.2)	341 (2.0)	>0.05
Coagulopathy	1064 (6.1)	54 (9.7)	1016 (6.0)	<0.05
Depression	2850 (16.5)	92 (16.6 )	2758 (16.5)	>0.05
Fluid and electrolyte disorder	5879 (33.9)	242 (43.7)	5637 (33.6)	<0.001
Pulmonary circulatory disorder	585 (3.4)	110 (19.9)	475 (2.8)	<0.001
Weight loss	2027 (11.7)	75 (13.5)	1952 (11.6)	>0.05

N/A: missing data.

LE DVT: Lower Extremity Deep Vein Thrombosis.

SCI: Spinal Cord Injury.

USD: United States Dollar.

Bolded values indicate statistical significance.

^aComparisons were conducted using the z-test with P-values adjusted using the Bonferroni method.

Among the 5333 patients with lumbar SCIs, 3.1% (n = 164) developed DVT. Patients were younger (42.2 ± 18.1 vs 46.3 ± 21.1 years, P < 0.001) and more likely to have pulmonary circulatory disorders (17.1% vs 2.5%, P < 0.001) than those without DVT (Table 4). Similar to the other SCIs, those with lumbar SCIs were more likely to have concomitant thrombotic complications, including pulmonary embolism (15.9% vs 1.4%, P < 0.001) and upper extremity DVT (2.4% vs 0.4%, P < 0.001) than those without DVT. No comorbidities were significantly associated with DVT risk. The details of additional comorbidities are summarized in Supplemental Table 1C.

Table 4.

Demographic Characteristics of Patients With Lumbar Spinal Cord Injury With or Without Lower Extremity Deep Vein Thrombosis Between 2016 and 2021 in the United States

Category	Total # of patients with lumbar SCI (N(%))	Lumbar SCI and LE DVT (N(%))	Lumbar SCI and no LE DVT (N(%))	P value^a
Number of admissions (N(%))	5333 (100)	164 (3.1)	5169 (96.9)	--
Mean age (yr)	46.1±21.0	42.2±18.1	46.3±21.1	<0.001
Sex (N(%))
Male	3681 (69.0)	136 (82.9)	3545 (68.6)	<0.001
Female	1649 (30.9)	28 (17.1)	1621 (31.4)	<0.001
N/A	3 (0.1)	0	3 (0.1)	>0.05
Race (N(%))
White	3102 (58.2)	80 (48.8)	3022 (58.5)	>0.05
Black	969 (18.2)	45 (27.4)	924 (17.9)	<0.05
Hispanic	703 (13.2)	45 (27.4)	924 (17.9)	>0.05
Asian or Pacific Islander	131 (2.5)	1 (0.6)	130 (2.5)	>0.05
Native American	37 (0.7)	0	37 (0.7)	>0.05
Other	181 (3.4)	8 (4.9)	173 (3.3)	>0.05
N/A	210 (3.9)	7 (4.3)	203 (3.9)	>0.05
Mean length of stay (days)	10.9±14.3	21.4±15.1	10.6±14.1	<0.001
Mean total charge (USD)	$165,486.9±$249,451.2	$337,071.1±$366,320.4	$160,022.3±$242,882.7	<0.001
Mean until first procedure (days)	2.0±7.2	3.3±7.1	1.9±7.2	>0.05
Mortality (N(%))
Died	93 (1.7)	1 (0.6)	92 (1.8)	>0.05
Did not die	5236 (98.2)	163 (99.4)	5073 (98.1)	>0.05
N/A	4 (0.1)	0	4 (0.1)	>0.05
Primary insurance (N(%))
Medicare	1568 (29.4)	24 (14.6)	1544 (29.9)	<0.001
Medicaid	1408 (26.4)	69 (42.1)	1339 (25.9)	>0.05
Private insurance	1537 (28.8)	49 (29.9)	1488 (28.8)	>0.05
Self-pay	355 (6.7)	10 (6.1)	345 (6.7)	>0.05
No charge	23 (0.4)	1 (0.6)	22 (0.4)	>0.05
Other	430 (8.1)	11 (6.7)	419 (8.1)	>0.05
N/A	12 (0.2)	0	12 (0.2)	>0.05
Smoking status
Yes	884 (16.6)	27 (16.5)	857 (16.6)	>0.05
No	4449 (83.4)	137 (83.5)	4312 (83.4)	>0.05
Concomitant injuries
Pulmonary embolism	99 (1.9)	26 (15.9)	73 (1.4)	<0.001
Upper extremity deep vein thrombosis	24 (0.5)	4 (2.4)	20 (0.4)	<0.01
Fracture of cervical spine	169 (3.2)	8 (4.9)	161 (3.1)	>0.05
Fracture of thoracic spine	788 (14.8)	35 (21.3)	753 (14.6)	>0.05
Fracture of lumbar spine	3066 (57.5)	114 (69.5)	2952 (57.1)	<0.05
Complete lesion of cervical spinal cord	0	0	0	NA
Complete lesion of thoracic spinal cord	24 (0.5)	1 (0.6)	23 (0.4)	>0.05
Complete lesion of lumbar spinal cord	234 (4.4)	11 (6.7)	223 (4.3)	>0.05
Incomplete lesion of cervical spinal cord	11 (0.2)	0	11 (0.2)	>0.05
Incomplete lesion of thoracic spinal cord	103 (1.9)	5 (3.0)	98 (1.9)	>0.05
Incomplete lesion of lumbar spinal cord	710 (13.3)	35 (21.3)	675 (13.1)	<0.05
Atrial fibrillation	378 (7.1)	10 (6.1)	368 (7.1)	>0.05
Cervical spinal cord injury	87 (1.6)	4 (2.4)	83 (1.6)	>0.05
Thoracic spinal cord injury	472 (8.9)	20 (12.2)	452 (8.7)	>0.05
Lumbar spinal cord injury	5333 (100)	164 (100)	5169 (100)	NA
Comorbidities
Acquired immune deficiency syndrome (AIDS)	87 (1.6)	3 (1.8)	84 (1.6)	>0.05
Coagulopathy	369 (6.9)	19 (11.6)	350 (6.8)	>0.05
Depression	781 (14.6)	15 (9.1)	766 (14.8)	>0.05
Fluid and electrolyte disorder	1519 (28.5)	70 (42.7)	1449 (28.0)	<0.05
Pulmonary circulatory disorder	155 (2.9)	28 (17.1)	127 (2.5)	<0.001
Weight loss	346 (6.5)	14 (8.5)	332 (6.4)	>0.05

N/A: missing data.

LE DVT: Lower Extremity Deep Vein Thrombosis.

SCI: Spinal Cord Injury.

USD: United States Dollar.

Bolded values indicate statistical significance.

^aComparisons were conducted using the z-test with P-values adjusted using the Bonferroni method.

Cervical SCI Risk Factors for DVT

Multivariate logistic regression analysis identified several significant risk factors associated with lower extremity DVT in patients with cervical SCI, including coagulopathies (Odds Ratio [OR]: 1.90, 95% Confidence Interval [CI]: 1.54-2.32, P < 0.001), complete cervical spinal cord lesions (OR: 1.84, CI: 1.43-2.35, P < 0.001), incomplete cervical spinal cord lesions (OR: 1.38, CI: 1.17-1.63, P < 0.01), concurrent cervical fractures (OR: 1.34, CI: 1.16-1.54, P < 0.01), concurrent lumbar fractures (OR: 1.58, CI: 1.17-2.11, P < 0.05), upper extremity DVT (OR: 3.58, CI: 2.53-4.97, P < 0.001), and pulmonary embolism (OR: 12.82, CI: 10.46-15.63, P < 0.001). Although older age was statistically significant (OR: 1.01, CI: 1.01-1.02, P < 0.001), its effect size was clinically negligible (Figure 1A).

Figure 1.

(A) Cervical: Multivariate Logistic Regression Adjusted for Age, Sex, Race, and Selected Factors. Note. Multivariate logistic regression adjusted for age, sex, year of admission, race, and selected comorbidities for cervical spine injury. Comparisons were conducted using the z-test with p-values adjusted using the Bonferroni method. Red dots denote statistically significant positive predictors based on odds ratio, while green dots denote statistically significant negative predictors. Bolded values indicate statistical significance. (B) Thoracic: Multivariate Logistic Regression Adjusted for Age, Sex, Race, and Selected Factors. Note. Multivariate logistic regression adjusted for age, sex, year of admission, race, and selected comorbidities for thoracic spine injury. Comparisons were conducted using the z-test with p-values adjusted using the Bonferroni method. Red dots denote statistically significant positive predictors based on odds ratio, while green dots denote statistically significant negative predictors. Bolded values indicate statistical significance. (C) Lumbar: Multivariate Logistic Regression Adjusted for Age, Sex, Race, and Selected Factors. Note.. Multivariate logistic regression adjusted for age, sex, year of admission, race, and selected comorbidities for lumbar spine injury. Comparisons were conducted using the z-test with p-values adjusted using the Bonferroni method. Red dots denote statistically significant positive predictors based on odds ratio, while green dots denote statistically significant negative predictors. Bolded values indicate statistical significance.

Thoracic SCI Risk Factors for DVT

Multivariate logistic regression analysis showed that upper extremity DVT (OR: 3.82, CI: 2.18 – 6.36, P < 0.001), pulmonary embolism (OR: 11.82, CI: 9.13 - 15.20, P < 0.001), thoracic fractures (OR: 1.46, CI: 1.20 – 1.77, P < 0.01), and fluid/electrolyte disorder (OR:1.35, CI:1.13-1.62, P < 0.05) were significantly associated with thoracic SCI and developing a lower extremity DVT (Figure 1B).

Lumbar SCI Risk Factors for DVT

Multivariate logistic regression analysis highlighted fluid and electrolyte disorders (OR: 1.92, CI: 1.38 – 2.66, P < 0.01), and pulmonary embolism (OR: 11.38, CI: 6.74-18.74, P < 0.001) as significantly associated with lumbar SCI and developing a lower extremity DVT (Figure 1C).

Outcomes

Patients with cervical SCI and lower extremity DVT also had increased length of stay (21.5 ± 23.6 vs 11.4 ± 15.9 days, P < 0.001), and higher total costs ($305,871.2 ± $379,281.4 vs $160,346.3 ± $251,422.9, P < 0.001) than those who did not develop DVT (Table 5).

Table 5.

Outcomes of Patients With Spinal Cord Injury With or Without Lower Extremity Deep Vein Thrombosis Between 2016 and 2021 in the United States

Category	Number of admissions (N(%))	Mean length of stay (days)	Mean total charge (USD)	Mean until first procedure (days)	Mortality (N(%))
Category	Number of admissions (N(%))	Mean length of stay (days)	Mean total charge (USD)	Mean until first procedure (days)	Died	Did not die
Total # of patients with cervical SCI (N(%))	36846 (100)	11.6 ± 16.2	$164,086.2 ± $256,539.1	2.4 ± 5.8	2074 (5.6)	34741 (94.3)
Cervical SCI and LE DVT (N(%))	956 (2.6)	21.5 ± 23.6	$305,871.2 ± $379,281.4	3.5 ± 6.7	75 (7.8)	881 (92.2)
Cervical SCI and no LE DVT (N(%))	35890 (97.4)	11.4 ± 15.9	$160,346.3 ± $251,422.9	2.4 ± 5.7	1999 (5.6)	33860 (94.3)
P value^a	--	<0.001	<0.001	<0.001	<0.001	<0.05
Total # of patients with thoracic SCI (N(%))	17319 (100)	11.9 ± 15.1	$156,243.1 ± $257,568.8	2.5 ± 5.4	448 (2.6)	16858 (97.3)
Thoracic SCI and LE DVT (N(%))	554 (3.2)	21.3 ± 23.2	$322,561.9 ± $449,922.5	3.8 ± 7.4	18 (3.2)	536 (96.8)
Thoracic SCI and no LE DVT (N(%))	16765 (96.8)	11.6 ± 14.7	$150,822.6 ± $246,956.2	2.4 ± 5.3	430 (2.6)	16322 (97.4)
P value^a	--	<0.001	<0.001	<0.001	>0.05	>0.05
Total # of patients with lumbar SCI (N(%))	5333 (100)	10.9 ± 14.3	$165,486.9 ± $249,451.2	2.0 ± 7.2	93 (1.7)	5236 (98.2)
Lumbar SCI and LE DVT (N(%))	164 (3.1)	21.4 ± 15.1	$337,071.1 ± $366,320.4	3.3 ± 7.1	1 (0.6)	163 (99.4)
Lumbar SCI and no LE DVT (N(%))	5169 (96.9)	10.6 ± 14.1	$160,022.3 ± $242,882.7	1.9 ± 7.2	92 (1.8)	5073 (98.1)
P value^a	--	<0.001	<0.001	>0.05	>0.05	>0.05

LE DVT: Lower Extremity Deep Vein Thrombosis.

SCI: Spinal Cord Injury.

USD: United States Dollar.

Bolded values indicate statistical significance.

^aComparisons were conducted using the z-test with P-values adjusted using the Bonferroni method.

Patients with thoracic SCI and lower extremity DVT also had increased length of stay (21.3 ± 23.2 days vs 11.6 ± 14.7 days, P < 0.001), and higher total costs ($322,561.9 ± $449,922.5 vs $150,822.6 ± $246,956.2, P < 0.001) compared to those without DVT (Table 5).

Patients with lumbar SCI and lower extremity DVT had increased length of stay (21.4 ± 15.1 days vs 10.6 ± 14.1 days, P < 0.001) and higher total costs ($337,071.1 ± $366,320.4 vs $160,023.3 ± $242,882.7, P < 0.001) compared to those without DVT (Table 5).

Mortality

Cervical SCI and the development of lower extremity DVT were associated with increased mortality (7.8% vs 5.6%, P < 0.001) compared to those who did not develop DVT (Table 5). No significant association between DVT and mortality was observed in the thoracic and lumbar SCI cohorts.

Discussion

Thromboembolic events, particularly DVT and PE, are major contributors to mortality among patients with SCI.^4,9,35 Although complications following SCI have been extensively investigated, there is a lack of robust analyses identifying DVT risk factors stratified by cervical, thoracic, and lumbar spinal injuries. In this national database analysis, we identified thoracic SCIs as having the highest DVT risk, followed by lumbar and cervical SCIs. Risk factors for DVT in cervical SCI included coagulopathies, advanced age, complete injuries, and concurrent cervical and lumbar fractures. In both cervical and thoracic SCIs, lower extremity DVT was associated with concomitant upper extremity DVT. In thoracic and lumbar SCIs, DVT was associated with fluid and electrolyte disturbances. Multivariate logistic regression - adjusted for age, sex, race, and selected factors - revealed that PE was a strong, independent predictor of lower extremity DVT in patients with cervical, thoracic, and lumbar SCIs.

Incidence

The overall incidence of DVT across all spinal injury levels in our study was 2.8%, which aligns with the 3.4% rate reported by Maung et al. in a large population-based analysis.²⁵ However, the reported DVT incidences in the SCI populations across all spinal levels vary widely in the remaining literature, ranging from 2% to 100%.^{5,6,21,22,36-39} These discrepancies may be attributed to limitations in earlier studies, including small sample sizes, single-institution designs, variations in prophylactic protocols, and heterogeneity in DVT screening methods.^{5,6,21,22,36-39}

Cervical SCIs constituted the largest cohort in our study yet had the lowest DVT incidence (2.6%) compared to lumbar (3.1%) and thoracic SCIs (3.2%). This lower incidence of cervical SCIs may be attributed to the higher mortality rates we observed associated with these injuries, reducing the number of survivors at risk for DVT. In contrast, thoracic or lumbar SCIs were not associated with increased mortality in our study. Consistent with our findings, DeVivo et al reported a relative risk of mortality of 11.1 for cervical SCIs at C1 to C3 compared to thoracic and lumbosacral injuries, suggesting survivor bias rather than indicating a true lower incidence of DVT in cervical SCI.⁴⁰ Thus, early mortality in patients with cervical SCIs may precede DVT onset and lead to underestimation of its incidence. Additionally, although current literature is limited in comparing prophylactic practices by injury level, it is possible that patients with cervical SCIs are more likely to receive early or aggressive prophylaxis, which could contribute to the lower observed DVT incidence.

Our findings underscore that the anatomical location of SCI influences DVT risk overall, with the strength of the association varying by injury level. While the present study’s level-specific differences in DVT incidence broadly align with prior investigations, there are differences in rank order.^15,25 Specifically, Maung et al. reported the highest DVT incidence in thoracic SCIs (5.1% for T1-T6 and 3.71% for T7-T12), followed by cervical (2.7% - 3.8% for C1-C4 and C5-C7, respectively), and then lumbar (2.53%).²⁵ However, Maung et al conducted their analysis using the National Trauma Data Bank (NTDB), which relies on voluntarily submitted data, limiting its national representativeness and validity for inferences on injury incidence and prevalence.^25,41,42 Conversely, Chung et al. found cervical SCI to carry the highest risk for DVT (HR = 2.96, 95% CI = 2.43, 3.61), followed by thoracic (HR = 2.68, 95% CI = 2.05, 3.50), and then lumbar SCI (HR = 1.60, 95% CI = 1.25, 2.05).¹⁵ While partially consistent with our findings, Chung et al.’s study utilized data derived from the Taiwan National Health Insurance Research Database, which may reflect geographic variations in SCI distribution and risk.

Shared Risk Factors Across SCI Levels

Common risk factors for DVT across all SCI levels align with Virchow’s triad, encompassing hypercoagulability, venous stasis, and endothelial injury.^43,44 Systemic complications such as pneumonia, sepsis, and multiple organ failure exacerbate hypercoagulability, while immobilization significantly contributes to venous stasis. These physiological effects are particularly prominent in higher-level spinal injuries, where the extent of neurological deficit and systemic dysregulation is greatest.^45-51 Consequently, the number of independent risk factors for DVT decreases progressively from cervical to lumbar injuries, reflecting the reduced motor and autonomic impairment at lower-level spinal injuries.

Upper extremity DVT was identified as a shared risk factor for lower extremity DVT in both cervical and thoracic SCI. This reflects the profound immobility, thrombotic risks associated with catheter use, and systemic hypercoagulability in high-level injuries. Unlike lumbar SCIs, upper cervical and thoracic SCIs may disrupt sympathetic outflow and impair systemic vascular tone, necessitating the use of central venous catheters and peripherally inserted catheters for hemodynamic stabilization.^52-54 These catheters can precipitate endothelial injury and worsen venous stasis, predisposing high-level SCI patients to thrombosis.^43,44,54-59

Furthermore, the loss of upper extremity and trunk mobility following cervical SCI and the loss of trunk mobility following thoracic SCI may further promote venous stasis.^60,61 This can increase the risk of upper extremity DVT, which is associated with concurrent lower extremity DVT in up to 16% of patients.⁵⁸

Our analysis found that both complete and incomplete lesions of the cervical and thoracic spine are independent risk factors for lower extremity DVT in cervical and thoracic SCI, respectively. This observation is consistent with prior studies, which report loss of motor function as a significant risk factor for VTE.^{6,14,22,23,25} Patients with American Spinal Injury Association Impairment Scale (AIS) A and B grades — indicating complete or incomplete loss of motor function—are particularly susceptible to DVT.^62,63 Higher-level SCIs often result in severe immobility,^2,61,64 leading to venous stasis in the lower extremities.⁶⁰ Additionally, autonomic dysregulation resulting from SCI at or above the T6 spinal level disrupts vascular tone, further promoting venous pooling.^45,65,66 This creates a prothrombotic environment as blood viscosity increases, increasing muscle hypoxia and decreased contractility.⁶⁷ These shared mechanisms may collectively underlie the elevated DVT risk in cervical and thoracic SCIs and highlight the importance of vigilant monitoring and proactive thromboprophylaxis in high-level SCIs to mitigate cascading thromboembolic events.

Cervical SCI Risk Factors

As described by multivariate analysis, patients with cervical SCIs possessed several unique risk factors for lower extremity DVT, including coagulopathy, older age, and concurrent fractures. While coagulopathy as a risk factor is not surprising, the association of coagulopathy with cervical SCIs, as opposed to thoracolumbar injuries, may be due to unique cardio-pulmonary impairment and the systemic complications of these lesions. In contrast to lower injury levels, cervical SCI often results in more pronounced respiratory impairment due to disruption of the diaphragm and accessory muscle innervation,^45,68,69 leading to respiratory muscle dysfunction^45,70 and a hypoxic environment that promotes fibrin deposition.^71-73 Furthermore, compared to thoracic and lumbar SCIs, cervical SCIs are more frequently associated with systemic complications such as sepsis, pneumonia, and multiple organ failure,^25,27,74 which can activate coagulation pathways and increase thrombotic risk.^75-78 For instance, Maung et al reported pneumonia in 51.1% of cervical SCI cases compared to only 18.9% in lumbar cases,²⁵ while Hoffman et al. observed higher rates of sepsis in cervical SCI but not in thoracic or lumbar SCIs.²⁷ Collectively, these findings suggest that a multifaceted pathophysiology associated with cervical SCIs heightens the DVT risk in these patients.

Older age was uniquely associated with DVT risk in cervical SCI, further emphasizing the vulnerability of this population. While age is a well-established risk factor for VTE, including DVT, in patients with SCI, this association has predominantly been established through studies that did not differentiate risk by injury level.^{14,15,20,21,25,79,80} Our findings suggest that specifically cervical-level injuries primarily drive the relationship between age and VTE in SCI. In elderly patients, the upper cervical levels are commonly injured,⁸¹ and inherent age-related changes such as increased thrombosis risk and venous insufficiency,^82,83 as well as cervical spine degeneration, may further predispose them to DVT.^84,85 In contrast, prior studies suggest that thoracic and lumbar SCIs occur predominantly in younger adults, which may explain why older age was not associated with DVT risk in these injury levels.^86,87

Thoracic SCI Risk Factors

Although thoracic SCI risk factors closely parallel those of cervical SCI, fluid and electrolyte disorders were an additional significant risk factor for patients with thoracic lesions. While prior studies have suggested that the level of injury does not influence electrolyte imbalances, these studies were limited by small sample sizes and did not distinguish between complete and incomplete lesions.^88,89 For injuries at the level of T6 and above, autonomic dysreflexia can disrupt blood pressure dysregulation and lead to renal dysfunction.⁹⁰ Meanwhile, injuries involving T10 to L1 directly impair renal innervation, resulting in electrolyte disorders from altered kidney function and renal deterioration,^91,92 which exacerbate inflammatory responses and promote VTE development.^93,94 Fluid and electrolyte disorders may be associated with DVT risk in thoracic but not cervical SCI due to the preserved compensatory mechanisms, such as anti-diuretic hormone release and activation of the renin-angiotensin-aldosterone system (RAAS) for incomplete cervical lesions.^95,96 In contrast, thoracic SCI disrupts the renal sympathetic nerves directly, impairing RAAS activation and further increasing the risk of DVT.

Lumbar SCI Risk Factors

Fluid and electrolyte imbalances were the primary contributors to DVT risk in patients with lumbar SCI. These findings are consistent with a study by Fineberg et al, which identified fluid electrolyte disorders as risk factors for developing both DVT and PE in patients undergoing lumbar spine surgery.⁹⁷ Although suboptimal renal perfusion and bladder innervation may contribute to fluid imbalances and DVT risk in both thoracic and lumbar SCIs, lumbar SCIs uniquely impair calf muscle pump activity, a key driver of venous return, leading to venous stasis.⁹⁸ Lumbar SCI had fewer predictive factors for lower extremity DVT than cervical and thoracic SCI. This difference may be attributed to the anatomical location of the conus medullaris, which terminates above L2, most commonly at the level of L1.^99-101 As a result, lumbar injuries are less likely to involve the spinal cord itself and may only partially disrupt vascular regulation, reducing the extent of autonomic dysfunction and immobility commonly associated with higher-level SCIs.

Outcomes

Patients with lower extremity DVT across all SCI levels experienced significantly prolonged hospital stays and increased healthcare costs compared to those without DVT. In cases of cervical SCI, the presence of DVT led to a significant increase in the average length of stay, while total hospital charges were significantly increased across cervical, thoracic, and lumbar regions. This highlights the considerable economic and resource burden of DVT in patients with SCI. Longer hospitalizations are likely due to the need for additional interventions to address thromboembolic complications, which include further imaging, anticoagulation treatment, and ongoing monitoring, as well as secondary complications such as pain and decreased mobility. Higher healthcare costs also arise from the need for specialized prophylaxis, diagnostic imaging, potential surgical interventions, along with the prolonged use of inpatient care facilities. Implementing early DVT prophylaxis, either immediately following an injury or preoperatively, may reduce incidence, shorten hospital stays, and decrease costs, ultimately optimizing hospital resource utilization while providing clinical benefits.

Clinical Implications

These findings emphasize the need for a proactive, risk-stratified approach to DVT management in patients with SCI. For individuals with a prior history of DVT, coagulopathy, or prolonged immobility, early preoperative screening, including targeted blood tests for clotting markers, could facilitate the timely identification of high-risk patients. Additionally, early and aggressive mobilization strategies for patients capable of ambulation should be prioritized as soon as clinically feasible. The strong association between lower extremity DVT and PE, in cervical SCI (OR: 12.82, CI: 10.46-15.63, P < 0.001), thoracic (OR: 11.82, CI: 9.13 - 15.20, P < 0.001), and lumbar (OR:11.38, CI: 6.74-18.74, P < 0.001) underscores the need for targeted prevention strategies. Although routine venous duplex ultrasonography is not currently recommended for DVT screening in all SCI patients, its selective use in high-risk cervical SCI patients may facilitate early detection and intervention.¹⁰² Additionally, extended-duration pharmacological prophylaxis may provide a benefit for those with persistent immobility or other risk factors for PE, such as cervical and thoracic SCIs, with some evidence supporting prophylaxis beyond 12 weeks.^103-105 However, further research is needed to determine the optimal duration of prophylaxis based on SCI level and recovery trajectory. In addition, electrolyte imbalances – particularly within the first two weeks of SCI – represent a significant yet underexplored risk factor for VTE.^88,89,106 Careful fluid management and renal monitoring may be an effective strategy to reduce DVT risk in thoracic and lumbar SCI patients. Such interventions must be weighed against the potential risks of bleeding and fluid overload, emphasizing the importance of individualized treatment plans informed by injury level, mobility status, and systemic comorbidities.

Limitations

The current study’s primary strength lies in its large sample size and nationally representative dataset across the United States. Nevertheless, this study has several limitations. As a retrospective analysis, the study is subject to biases, including potential underreporting, misclassification, and missing data, which may impact the findings. Additionally, use of the NIS database has inherent limitations, including the absence of detailed clinical information such as physical and neurological exam findings, imaging results, and biomarker data to inform diagnostic accuracy. Furthermore, DVT screening methods may differ across different institutions, introducing heterogeneity in DVT identification rates.^{5,6,21,22,36-39} Another limitation is the lack of detailed temporal information on diagnoses, chronic conditions, and comorbidities, making it challenging to establish clear causal relationships. Additionally, databases typically do not routinely gather granular information such as the precise treatment regimen used, complications encountered during treatment, the patient’s functional and neurological status, and the AIS grades, all of which can provide insight into additional risk factors. While stratifying SCI according to AIS grading would have provided additional insight into additional risk factors, this was not feasible due to the limitations of ICD coding, which does not directly correspond to AIS classifications. Although it can be reasonably inferred that a complete lesion aligns with AIS-A, further differentiation (eg, AIS-B, C, D, E) requires detailed neurological examinations or specific documentation that was not available in the NIS. This restricts our ability to correlate the level of functional impairment with thromboembolic risk in SCI patients. Additionally, neurologic injury was identified using SCI-related diagnostic codes, which may not fully capture non-SCI causes of motor impairment (eg, stroke) that influence thrombotic risk. Furthermore, the NIS database provides only a limited view of each patient’s index admission and de-identifies all personal identifiers, resulting in each readmission being documented as an independent, new admission, thus potentially leading to an overestimation of rates. Despite these limitations, we performed multivariate analyses to control for confounding variables, offering the largest nationwide dataset analysis on identifying risk factors for DVT in SCI.

Conclusion

In our analysis, we identified critical risk factors for DVT in patients across different SCI levels. Using the NIS, we stratified DVT risk factors for cervical, thoracic, and lumbar SCI, demonstrating significant variability in risk based on injury level. Prior studies have largely combined all SCI levels or focused predominantly on cervical injuries, overlooking the distinct nuances in DVT risk associated with injury level. Specifically, thoracic SCI was associated with the highest incidence of DVT, followed by lumbar and cervical SCIs, with each level presenting unique risk factors. Patients with higher-level SCIs may benefit from earlier initiation or extended DVT prophylaxis and screening, whereas those with lower-level SCIs may require additional monitoring and management of fluid and electrolyte imbalances to reduce thrombotic risk. By using the NIS, a large national database, our study offers robust statistical power and broad generalizability, addressing the limitations of previous studies that likely reflected regional patterns. Our findings underscore the importance of tailored DVT prophylactic strategies based on SCI level and offer evidence for refining DVT risk stratification in SCI patients. Future studies should confirm these associations and validate the efficacy of SCI level-based DVT prophylactic interventions.

Supplemental Material

Supplemental Material - Risk Factors for Lower Extremity Deep Vein Thrombosis by Spinal Cord Injury Level: A Population-Based Analysis

Supplemental Material for Risk Factors for Lower Extremity Deep Vein Thrombosis by Spinal Cord Injury Level: A Population-Based Analysis by Alejandro Pando, MD, PhD, Caryn J. Ha, MSc, Yaxel Levin-Carrion, BA, Ahmed Sabra, BA, Max Ward, MD, Daniel M. Schneider, MD, Drew Thibault, DO, Sheng-fu Larry Lo, MD, and Daniel M. Sciubba, MD, MBA in Global Spine Journal.

Footnotes

ORCID iDs

Caryn J. Ha

Daniel M. Schneider

Ethical Considerations

The NIS is a deidentified administrative database exempt from the Institutional Review Board approval and informed consent requirements.

Author Contributions

Alejandro Pando: conceptualization, methodology, formal analysis, investigation, writing – original draft, writing – review & editing; Caryn J. Ha: conceptualization, formal analysis, investigation, writing – original draft, writing – review & editing; Yaxel Levin-Carrion: investigation, writing – original draft, writing – review & editing; Ahmed Sabra: investigation, writing – original draft, writing – review & editing; Max Ward: methodology, writing – review & editing; Daniel M. Schneider: methodology, writing – review & editing; Sheng-fu Larry Lo: conceptualization, writing – review & editing; Daniel M. Sciubba: conceptualization, writing – review & editing.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

Declaration of Conflicting Interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Data Availability Statement

The data that support the finding of this study are available from the first author (AP) upon reasonable request.*

Supplemental Material

Supplemental material for this article is available online.

References

Alizadeh

Dyck

Karimi-Abdolrezaee

. Traumatic spinal cord injury: an overview of pathophysiology, models and acute injury mechanisms. Front Neurol. 2019;10:282. doi:10.3389/fneur.2019.00282

Ahuja

Wilson

Nori

, et al. Traumatic spinal cord injury. Nat Rev Dis Primers. 2017;3:17018. doi:10.1038/nrdp.2017.18

Jain

Ayers

Peterson

, et al. Traumatic spinal cord injury in the United States, 1993-2012. JAMA. 2015;313(22):2236-2243. doi:10.1001/jama.2015.6250

Middleton

Dayton

Walsh

Rutkowski

Leong

Duong

. Life expectancy after spinal cord injury: a 50-year study. Spinal Cord. 2012;50(11):803-811. doi:10.1038/sc.2012.55

Geerts

Code

Jay

Chen

Szalai

. A prospective study of venous thromboembolism after major trauma. N Engl J Med. 1994;331(24):1601-1606. doi:10.1056/NEJM199412153312401

Myllynen

Kammonen

Rokkanen

Bostman

Lalla

Laasonen

. Deep venous thrombosis and pulmonary embolism in patients with acute spinal cord injury: a comparison with nonparalyzed patients immobilized due to spinal fractures. J Trauma. 1985;25(6):541-543. doi:10.1097/00005373-198506000-00013

Todd

Frisbie

Rossier

, et al. Deep venous thrombosis in acute spinal cord injury: a comparison of 125I fibrinogen leg scanning, impedance plethysmography and venography. Paraplegia. 1976;14(1):50-57. doi:10.1038/sc.1976.8

DeVivo

Kartus

Stover

Rutt

Fine

. Cause of death for patients with spinal cord injuries. Arch Intern Med. 1989;149(8):1761-1766.

DeVivo

Krause

Lammertse

. Recent trends in mortality and causes of death among persons with spinal cord injury. Arch Phys Med Rehabil. 1999;80(11):1411-1419. doi:10.1016/s0003-9993(99)90252-6

10.

Shavelle

DeVivo

Brooks

Strauss

Paculdo

. Improvements in long-term survival after spinal cord injury? Arch Phys Med Rehabil. 2015;96(4):645-651. doi:10.1016/j.apmr.2014.11.003

11.

DeVivo

. Sir Ludwig Guttmann Lecture: trends in spinal cord injury rehabilitation outcomes from model systems in the United States: 1973-2006. Spinal Cord. 2007;45(11):713-721. doi:10.1038/sj.sc.3102026

12.

Munoz

Mismetti

Poggio

, et al. Clinical outcome of patients with upper-extremity deep vein thrombosis: results from the RIETE Registry. Chest. 2008;133(1):143-148. doi:10.1378/chest.07-1432

13.

Owens

Bui

Knuttinen

Gaba

Carrillo

. Pulmonary embolism from upper extremity deep vein thrombosis and the role of superior vena cava filters: a review of the literature. J Vasc Intervent Radiol. 2010;21(6):779-787. doi:10.1016/j.jvir.2010.02.021

14.

Jones

Ugalde

Franks

Zhou

White

. Venous thromboembolism after spinal cord injury: incidence, time course, and associated risk factors in 16,240 adults and children. Arch Phys Med Rehabil. 2005;86(12):2240-2247. doi:10.1016/j.apmr.2005.07.286

15.

Chung

Lin

Chang

Chung

Sung

Kao

. Increased risk of deep vein thrombosis and pulmonary thromboembolism in patients with spinal cord injury: a nationwide cohort prospective study. Thromb Res. 2014;133(4):579-584. doi:10.1016/j.thromres.2014.01.008

16.

Giorgi Pierfranceschi

Donadini

Dentali

, et al. The short- and long-term risk of venous thromboembolism in patients with acute spinal cord injury: a prospective cohort study. Thromb Haemost. 2013;109(1):34-38. doi:10.1160/TH12-06-0390

17.

Godat

Kobayashi

Chang

Coimbra

. Can we ever stop worrying about venous thromboembolism after trauma? J Trauma Acute Care Surg. 2015;78(3):475-480. doi:10.1097/TA.0000000000000556. discussion 480-1.

18.

Clements

Churilov

Wahab

. Exploratory analysis of factors associated with venous thromboembolism in Victorian acute traumatic spinal cord-injured patients 2010–2013. Spinal Cord. 2017;55(1):74-78. doi:10.1038/sc.2016.94

19.

Rossi

Green

Rosen

Spies

Jao

. Sequential changes in factor VIII and platelets preceding deep vein thrombosis in patients with spinal cord injury. Br J Haematol. 1980;45(1):143-151. doi:10.1111/j.1365-2141.1980.tb03819.x

20.

Watson

. Venous thrombosis and pulmonary embolism in spinal cord injury. Paraplegia. 1968;6(3):113-121. doi:10.1038/sc.1968.21

21.

Shang

Wanyan

Zhang

Wang

. Incidence and risk factors of deep vein thrombosis in patients with spinal cord injury: a systematic review with meta-analysis. Front Cardiovasc Med. 2023;10:1153432. doi:10.3389/fcvm.2023.1153432

22.

Waring

Karunas

. Acute spinal cord injuries and the incidence of clinically occurring thromboembolic disease. Paraplegia. 1991;29(1):8-16. doi:10.1038/sc.1991.2

23.

Wei

Zhou

Liu

, et al. Risk factors for venous thromboembolism in patients with spinal cord injury: a systematic review and meta-analysis. J Spinal Cord Med. 2023;46(2):181-193. doi:10.1080/10790268.2021.1913561

24.

Selassie

Varma

Saunders

. Current trends in venous thromboembolism among persons hospitalized with acute traumatic spinal cord injury: does early access to rehabilitation matter? Arch Phys Med Rehabil. 2011;92(10):1534-1541. doi:10.1016/j.apmr.2011.04.018

25.

Maung

Schuster

Kaplan

Maerz

Davis

. Risk of venous thromboembolism after spinal cord injury: not all levels are the same. J Trauma. 2011;71(5):1241-1245. doi:10.1097/TA.0b013e318235ded0

26.

Ploumis

Yadlapalli

Fehlings

Kwon

Vaccaro

. A systematic review of the evidence supporting a role for vasopressor support in acute SCI. Spinal Cord. 2010;48(5):356-362. doi:10.1038/sc.2009.150

27.

Hoffman

Hauser

Zaki

, et al. Spinal level and cord involvement in the prediction of sepsis development after vertebral fracture repair for traumatic spinal injury. J Neurosurg Spine. 2022;37(2):292-298. doi:10.3171/2021.12.SPINE21423

28.

(HCUP) HCaUP . HCUP Databases. Agency for Healthcare Research and Quality. 2024. https://www.hcup-us.ahrq.gov/nisoverview.jsp. Accessed 26 September 2024. Updated.

29.

(HCUP) HCaUP . Producing national HCUP estimates - accessible version. Agency for healthcare research and quality. 2018. https://www.hcup-us.ahrq.gov/tech_assist/nationalestimates/508_course/508course_2018.jsp. Accessed 26 September 2024.

30.

(HCUP) HCaUP . HCUP Frequently Asked Questions. Agency for Healthcare Research and Quality. 2024. https://www.hcup-us.ahrq.gov/tech_assist/faq.jsp. Accessed September 26, 2024.

31.

Release of the 2015 National Inpatient Sample (NIS). Agency for Healthcare Research and Quality. 2024. https://hcup-us.ahrq.gov/news/announcements/nis_111517.jsp

32.

Elixhauser

Steiner

Harris

Coffey

. Comorbidity measures for use with administrative data. Med Care. 1998;36(1):8-27. doi:10.1097/00005650-199801000-00004

33.

Waters

Adkins

Yakura

. Definition of complete spinal cord injury. Paraplegia. 1991;29(9):573-581. doi:10.1038/sc.1991.85

34.

Rupp

Biering-Sørensen

Burns

, et al. International standards for neurological classification of spinal cord injury: revised 2019. Top Spinal Cord Inj Rehabil. 2021;27(2):1-22. doi:10.46292/sci2702-1

35.

Hagen

Aarli

Gronning

. The clinical significance of spinal cord injuries in patients older than 60 years of age. Acta Neurol Scand. 2005;112(1):42-47. doi:10.1111/j.1600-0404.2005.00430.x

36.

Aito

Pieri

D'Andrea

Marcelli

Cominelli

. Primary prevention of deep venous thrombosis and pulmonary embolism in acute spinal cord injured patients. Spinal Cord. 2002;40(6):300-303. doi:10.1038/sj.sc.3101298

37.

Grossman

Frankowski

Burau

, et al. Incidence and severity of acute complications after spinal cord injury. J Neurosurg Spine. 2012;17(1 Suppl):119-128. doi:10.3171/2012.5.AOSPINE12127

38.

Watson

. Anticoagulant therapy in the treatment of venous thrombosis and pulmonary embolism in acute spinal injury. Paraplegia. 1974;12(3):197-201. doi:10.1038/sc.1974.31

39.

Gunduz

Ogur

Mohur

Somuncu

Acjksoz

Ustunsoz

. Deep vein thrombosis in spinal cord injured patients. Paraplegia. 1993;31(9):606-610. doi:10.1038/sc.1993.96

40.

DeVivo

Stover

Black

. Prognostic factors for 12-year survival after spinal cord injury. Arch Phys Med Rehabil. 1992;73(2):156-162.

41.

Hashmi

Kaji

Nathens

. Practical guide to surgical data sets: national trauma data bank (NTDB). JAMA Surg. 2018;153(9):852-853. doi:10.1001/jamasurg.2018.0483

42.

Trauma ACoSCo . National trauma data bank (NTDB), annual report 2007. Version 7.0. https://www.ntdb.org

43.

McLendon

KGA

Attia

. Deep venous thrombosis risk factors. In: StatPearls. StatPearls Publishing; 2023. https://www.ncbi.nlm.nih.gov/books/NBK470215/

44.

Kumar

Hanlin

Glurich

Mazza

Yale

. Virchow's contribution to the understanding of thrombosis and cellular biology. Clin Med Res. 2010;8(3-4):168-172. doi:10.3121/cmr.2009.866

45.

Krassioukov

. Autonomic function following cervical spinal cord injury. Respir Physiol Neurobiol. 2009;169(2):157-164. doi:10.1016/j.resp.2009.08.003

46.

Krassioukov

Claydon

. The clinical problems in cardiovascular control following spinal cord injury: an overview. Prog Brain Res. 2006;152:223-9229. doi:10.1016/S0079-6123(05)52014-4

47.

McKinley

Garstang

Wieting

, . Cardiovascular concerns in spinal cord injury. Cord Injury: eMedicine Specialties/Physical Medicine and Rehabilitation/Spinal 2006.

48.

Glenn

Bergman

. Cardiovascular changes following spinal cord injury. Top Spinal Cord Inj Rehabil. 1997;2(4):47-53.

49.

Lehmann

Lane

Piepmeier

Batsford

. Cardiovascular abnormalities accompanying acute spinal cord injury in humans: incidence, time course and severity. J Am Coll Cardiol. 1987;10(1):46-52. doi:10.1016/s0735-1097(87)80158-4

50.

Piepmeier

Lehmann

Lane

. Cardiovascular instability following acute cervical spinal cord trauma. Cent Nerv Syst Trauma. 1985;2(3):153-160. doi:10.1089/cns.1985.2.153

51.

Winslow

Lesch

Talano

Meyer

Jr . Spinal cord injuries associated with cardiopulmonary complications. Spine. 1986;11(8):809-812. doi:10.1097/00007632-198610000-00014

52.

Stevens

Bhardwaj

Kirsch

Mirski

. Critical care and perioperative management in traumatic spinal cord injury. J Neurosurg Anesthesiol. 2003;15(3):215-229. doi:10.1097/00008506-200307000-00009

53.

Bilello

Davis

Cunningham

Groom

Lemaster

Sue

. Cervical spinal cord injury and the need for cardiovascular intervention. Arch Surg. 2003;138(10):1127-1129. doi:10.1001/archsurg.138.10.1127

54.

Onmez

Cingoz

Kucuksen

, et al. Bilateral upper-extremity deep vein thrombosis following central cord syndrome. J Spinal Cord Med. 2013;36(3):243-246. doi:10.1179/2045772313Y.0000000096

55.

Spencer

Emery

Lessard

Goldberg

Worcester Venous Thromboembolism S . Upper extremity deep vein thrombosis: a community-based perspective. Am J Med. 2007;120(8):678-684. doi:10.1016/j.amjmed.2006.06.046

56.

Grant

Stevens

Woller

, et al. Diagnosis and management of upper extremity deep-vein thrombosis in adults. Thromb Haemost. 2012;108(6):1097-1108. doi:10.1160/TH12-05-0352

57.

Heil

Miesbach

Vogl

Bechstein

Reinisch

. Deep vein thrombosis of the upper extremity. Dtsch Arztebl Int. 2017;114(14):244-249. doi:10.3238/arztebl.2017.0244

58.

Lee

Zierler

. The risk factors and clinical outcomes of upper extremity deep vein thrombosis. Vasc Endovasc Surg. 2012;46(2):139-144. doi:10.1177/1538574411432145

59.

Hyman

Cardenas

. Upper-extremity deep vein thrombosis associated with peripherally inserted central catheters in acute spinal cord injury: a report of 2 cases. Arch Phys Med Rehabil. 2002;83(9):1313-1316. doi:10.1053/apmr.2002.33642

60.

Merli

Crabbe

Paluzzi

Fritz

. Etiology, incidence, and prevention of deep vein thrombosis in acute spinal cord injury. Arch Phys Med Rehabil. 1993;74(11):1199-1205.

61.

Bennett

JDJ

Emmady

. Spinal Cord Injuries. StatPearls Publishing. Updated 2024 Mar 10. https://www.ncbi.nlm.nih.gov/books/NBK560721/

62.

Qin

, et al. Incidence and risk factors predicting deep venous thrombosis of lower extremity following spinal fractures. Sci Rep. 2021;11(1):2441. doi:10.1038/s41598-021-82147-x

63.

Wang

. Risk factors for postoperative DVT exacerbation or new DVT in patients with spinal cord injury complicated with cervical fracture. Front Cardiovasc Med. 2024;11:1458941. doi:10.3389/fcvm.2024.1458941

64.

Mathias

. 81 - autonomic disturbances in spinal cord injuries. In: Robertson

Biaggioni

Burnstock

Low

, eds. Primer on the Autonomic Nervous System. 2nd ed. Academic Press; 2004:298-301.

65.

Sidorov

Townson

Dvorak

Kwon

Steeves

Krassioukov

. Orthostatic hypotension in the first month following acute spinal cord injury. Spinal Cord. 2008;46(1):65-69. doi:10.1038/sj.sc.3102064

66.

Claydon

Steeves

Krassioukov

. Orthostatic hypotension following spinal cord injury: understanding clinical pathophysiology. Spinal Cord. 2006;44(6):341-351. doi:10.1038/sj.sc.3101855

67.

Kim

Park

Kim

. Cardiac arrest attributable to dysfunction of the autonomic nervous system after traumatic cervical spinal cord injury. Chin J Traumatol (Engl Ed). 2017;20(2):118-121. doi:10.1016/j.cjtee.2016.11.004

68.

Benditt

. Pathophysiology of neuromuscular respiratory Diseases. Clin Chest Med. 2018;39(2):297-308. doi:10.1016/j.ccm.2018.01.011

69.

Brown

DiMarco

Hoit

Garshick

. Respiratory dysfunction and management in spinal cord injury. Respir Care. 2006;51(8):853-868. discussion 869-70.

70.

Galeiras Vazquez

Rascado Sedes

Mourelo Farina

Montoto Marques

Ferreiro Velasco

. Respiratory management in the patient with spinal cord injury. BioMed Res Int. 2013;2013:168757. doi:10.1155/2013/168757

71.

Yan

Mackman

Kisiel

Stern

Pinsky

. Hypoxia/Hypoxemia-Induced activation of the procoagulant pathways and the pathogenesis of ischemia-associated thrombosis. Arterioscler Thromb Vasc Biol. 1999;19(9):2029-2035. doi:10.1161/01.atv.19.9.2029

72.

Gupta

Sahu

Prabhakar

, et al. Activation of NLRP3 inflammasome complex potentiates venous thrombosis in response to hypoxia. Proc Natl Acad Sci USA. 2017;114(18):4763-4768. doi:10.1073/pnas.1620458114

73.

Gupta

Zhao

Evans

. The stimulation of thrombosis by hypoxia. Thromb Res. 2019;181:77-83. doi:10.1016/j.thromres.2019.07.013

74.

Stein

Menaker

McQuillan

Handley

Aarabi

Scalea

. Risk factors for organ dysfunction and failure in patients with acute traumatic cervical spinal cord injury. Neurocritical Care. 2010;13(1):29-39. doi:10.1007/s12028-010-9359-9

75.

Fourrier

Chopin

Goudemand

, et al. Septic shock, multiple organ failure, and disseminated intravascular coagulation. Compared patterns of antithrombin III, protein C, and protein S deficiencies. Chest. 1992;101(3):816-823. doi:10.1378/chest.101.3.816

76.

Levi

van der Poll

. Coagulation and sepsis. Thromb Res. 2017;149:38-44. doi:10.1016/j.thromres.2016.11.007

77.

Vail

Xie

Haney

Barnes

. Biomarkers of thrombosis, fibrinolysis, and inflammation in patients with severe sepsis due to community-acquired pneumonia with and without Streptococcus pneumoniae. Infection. 2009;37(4):358-364. doi:10.1007/s15010-008-8128-6

78.

Violi

Cangemi

Calvieri

. Pneumonia, thrombosis and vascular disease. J Thromb Haemostasis. 2014;12(9):1391-1400. doi:10.1111/jth.12646

79.

Zhang

Fang

Pang

, et al. Association between age and incidence of deep vein thrombosis in patients with spinal cord injury: an observational cross-sectional study. Spinal Cord. 2022;60(11):1006-1013. doi:10.1038/s41393-022-00814-w

80.

Piran

Schulman

. Incidence and risk factors for venous thromboembolism in patients with acute spinal cord injury: a retrospective study. Thromb Res. 2016;147:97-101. doi:10.1016/j.thromres.2016.09.030

81.

Futch

Seas

Ononogbu-Uche

, et al. Shifting trends in the epidemiology of cervical spine injuries: an analysis of 11,822 patients from the national electronic injury surveillance system over two decades. J Neurotrauma. 2024;41(17-18):2158-2167. doi:10.1089/neu.2024.0194

82.

Kakkar

Howe

Nicolaides

Renney

JTG

Clarke

. Deep vein thrombosis of the leg: is there a “high risk” group? Am J Surg. 1970;120(4):527-530. doi:10.1016/S0002-9610(70)80023-X

83.

Engbers

van Hylckama

Rosendaal

. Venous thrombosis in the elderly: incidence, risk factors and risk groups. J Thromb Haemostasis. 2010;8(10):2105-2112. doi:10.1111/j.1538-7836.2010.03986.x

84.

White

Panjabi

. Clinical biomechanics of the spine. Philadelphia, PA: JB Lippincott Co.;1978.

85.

Zhang

Wang

. Traumatic spinal cord injury caused by low falls and high falls: a comparative study. J Orthop Surg Res. 2021;16(1):222. doi:10.1186/s13018-021-02379-5

86.

Selvarajah

Hammond

Haider

, et al. The burden of acute traumatic spinal cord injury among adults in the United States: an update. J Neurotrauma. 2014;31(3):228-238. doi:10.1089/neu.2013.3098

87.

Thompson

Mutch

Parent

Mac-Thiong

. The changing demographics of traumatic spinal cord injury: an 11-year study of 831 patients. J Spinal Cord Med. 2015;38(2):214-223. doi:10.1179/2045772314Y.0000000233

88.

Peruzzi

Shapiro

Meyer

Jr Krumlovsky

Seo

. Hyponatremia in acute spinal cord injury. Crit Care Med. 1994;22(2):252-258. doi:10.1097/00003246-199402000-00016

89.

Chavasiri

Suriyachat

Luksanapruksa

Wilartratsami

Chavasiri

. Incidence of and factors associated with hyponatremia in traumatic cervical spinal cord injury patients. Spinal Cord Ser Cases. 2022;8(1):15. doi:10.1038/s41394-022-00475-0

90.

Lakra

Swayne

Christofi

Desai

. Autonomic dysreflexia in spinal cord injury. Pract Neurol. 2021;21(6):532-538. doi:10.1136/practneurol-2021-002956

91.

Wulf

Tom

. Consequences of spinal cord injury on the sympathetic nervous system. Front Cell Neurosci. 2023;17:999253. doi:10.3389/fncel.2023.999253

92.

Elmelund

Oturai

Toson

Biering-Sorensen

. Forty-five-year follow-up on the renal function after spinal cord injury. Spinal Cord. 2016;54(6):491. doi:10.1038/sc.2016.2

93.

Wilck

Balogh

Marko

Bartolomaeus

Muller

. The role of sodium in modulating immune cell function. Nat Rev Nephrol. 2019;15(9):546-558. doi:10.1038/s41581-019-0167-y

94.

Temraz

Tamim

Mailhac

Taher

. Could sodium imbalances predispose to postoperative venous thromboembolism? An analysis of the NSQIP database. Thromb J. 2018;16:11. doi:10.1186/s12959-018-0165-5

95.

Sved

McDowell

Blessing

. Release of antidiuretic hormone in quadriplegic subjects in response to head-up tilt. Neurology. 1985;35(1):78-82. doi:10.1212/wnl.35.1.78

96.

Katzelnick

Weir

Pinto

, et al. Increased pulse wave velocity in persons with spinal cord injury: the effect of the renin-angiotensin-aldosterone system. Am J Physiol Heart Circ Physiol. 2021;320(1):H272-H280. doi:10.1152/ajpheart.00544.2020

97.

Fineberg

Oglesby

Patel

Pelton

Singh

. The incidence and mortality of thromboembolic events in lumbar spine surgery. Spine. 2013;38(13):1154-1159. doi:10.1097/BRS.0b013e318286b7c0

98.

Miller

Pegelow

Jacques

Dempsey

. Skeletal muscle pump versus respiratory muscle pump: modulation of venous return from the locomotor limb in humans. J Physiol. 2005;563(Pt 3):925-943. doi:10.1113/jphysiol.2004.076422

99.

Malas

Seker

Salbacak

Buyukmumcu

Karabulut

Yardimci

. The relationship between the lumbosacral enlargement and the conus medullaris during the period of fetal development and adulthood. Surg Radiol Anat. 2000;22(3-4):163-168. doi:10.1007/s00276-000-0163-7

100.

Saifuddin

Burnett

White

. The variation of position of the conus medullaris in an adult population. A magnetic resonance imaging study. Spine. 1998;23(13):1452-1456. doi:10.1097/00007632-199807010-00005

101.

Elfiky

El Mansy

Stienen

Yunusa

Elkaref

Nafady

. Magnetic resonance imaging-based anatomy of the conus medullaris: variations of location and morphology. World Neurosurg. 2025;195:123646. doi:10.1016/j.wneu.2024.123646

102.

Geerts

Pineo

Heit

, et al. Prevention of venous thromboembolism: the seventh ACCP conference on antithrombotic and thrombolytic therapy. Chest. 2004;126(3 Suppl):338S-400S. doi:10.1378/chest.126.3_suppl.338S

103.

Spinal Cord Injury Thromboprophylaxis I . Prevention of venous thromboembolism in the rehabilitation phase after spinal cord injury: prophylaxis with low-dose heparin or enoxaparin. J Trauma. 2003;54(6):1111-1115. doi:10.1097/01.TA.0000042159.90102.C2

104.

Weidner

Muller

Hach-Wunderle

, et al. Prevention of thromboembolism in spinal cord injury -S1 guideline. Neurol Res Pract. 2020;2:43. doi:10.1186/s42466-020-00089-7

105.

Dhall

Hadley

Aarabi

, et al. Deep venous thrombosis and thromboembolism in patients with cervical spinal cord injuries. Neurosurgery. 2013;72(Suppl 2):244-254. doi:10.1227/NEU.0b013e31827728c0

106.

Salazar

LRM

Agrawal

Satyarthee

, et al. Hyponatremia in the acute phase of spinal cord trauma: review. J Acute Dis. 2018;7(3):103-107. doi:10.4103/2221-6189.236823

Supplementary Material

Please find the following supplemental material available below.

For Open Access articles published under a Creative Commons License, all supplemental material carries the same license as the article it is associated with.

For non-Open Access articles published, all supplemental material carries a non-exclusive license, and permission requests for re-use of supplemental material or any part of supplemental material shall be sent directly to the copyright owner as specified in the copyright notice associated with the article.

0.00 MB

0.03 MB