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Incidence and Outcome of Vertebral Artery Dissection in Trauma Setting: Analysis of National Trauma Data Base

Abstract

Background

The natural history and epidemiological aspects of traumatic vertebral artery dissection (VAD) are not fully understood. We determined the prevalence of VAD and impact on outcome of patients with head and neck trauma.

Methods

All the patients who were admitted with traumatic brain injury or head and neck trauma were identified by ICD-9-CM codes from the National Trauma Data Bank (NTDB), using data files from 2009 to 2010. NTDB represents one of the largest trauma databases and contains data from over 900 trauma centers across the United States. Presence of VAD was identified in these patients by using ICD-9-CM codes. Admission Glasgow Coma Scale (GCS) score, injury severity score (ISS), in-hospital complications, and treatment outcome were compared between patients with and without VAD.

Results

A total of 84 VAD patients were identified which comprised 0.01 % of all patients admitted with head and neck trauma. The mean age (in years) for patients with VAD was significantly higher than patients without dissection [46 (95 % CI 41–50) vs. 41.3 (95 % CI 41.2–41.4); p = 0.003]. The proportion of patients presenting with GCS score <9 was significantly higher in patients with VAD (31 vs. 12 %, p < 0.0001). The rate of cervical vertebral fracture was significantly higher in patients with VAD (71 vs. 11 %, p < 0.0001). Patients with VAD had higher rates of in-hospital stroke than patients without dissection (5 vs. 0.2 %, p < 0.0001). Numbers of ICU days, ventilator days, and hospital length of stays were all significantly higher in patients with VAD. These differences remained significant after adjusting for the demographics, admission GCS score, and ISS (p < 0.0001). A total of 7 % (N = 6) of the patients with VAD received endovascular treatment and there was no in-hospital stroke in these patients. Patients with VAD had a higher chance of discharge to nursing facilities in comparison to head trauma patients without VAD (OR: 2.1; 95 % CI 1.4–3.5; p < 0.0001).

Conclusion

Although infrequent, VAD in head and neck trauma is associated with higher rates of in-hospital stroke and longer length of ICU stay and total hospital stay. Early diagnosis and endovascular treatment may be an alternative option to reduce the rate of in-hospital stroke in these patients.

Introduction

Despite the advancements in the care of patients with head and neck trauma [1], the criteria for screening of blunt cervical arterial injury and associated clinical events are understudied [2]. Paucity of data is particularly prominent in regards to vertebral artery dissection (VAD) which occurs due to rapid acceleration–deceleration injury causing rotation and hyperextension of the neck within the scope of trauma [3]. Our understanding of the rate of cerebral ischemic events and need for endovascular or surgical treatment in these patients is based on anecdotal data. Data derived from multiple institutions is required to provide higher precision of estimates regarding clinical events, treatments, and outcomes and to ensure generalizability of findings [4, 5].

In this study, we determined the prevalence of traumatic VAD and associated hospital events, treatments, and outcomes in patients with head and neck trauma and traumatic brain injury, using a nationally representative database.

Methods

Study Population

Patients entered in National Trauma Data Bank (NTDB) between January 1st, 2009 and December 31st, 2010 were analyzed. NTBD is the largest and the most complete trauma database compiled by American College of Surgeons in the United States. This database contains uniformly collected clinical, demographic, and external cause and outcome information on over three million cases from over 900 registered U.S. trauma centers [6].

All the patients who were admitted to hospitals with traumatic brain injury or head and neck trauma were identified using the international classification of diseases, ninth revision, clinical modification (ICD-9-CM) diagnosis codes for traumatic brain injury (800.0–801.99, 803.0–804.99 or 850.0–854.19), head and neck injury (802, 802.0–802.9, 802.20–802.39), and cervical spine fracture (805.0, 805.00–805.08, 805.1, 805.10–805.18, 806.1, 806.0, 806.00 and 806.01–806.19) similar to the previously published studies [68].

Study Variables

Variables including patient’s demographics, admission injury severity score (ISS), Glasgow Coma Scale (GCS) score, in-hospital complications such as stroke (defined as an embolic, thrombotic, or hemorrhagic vascular accident or stroke with motor sensory or cognitive dysfunction that persists for 24 or more hours), myocardial infarction, pneumonia and deep vein thrombosis, and outcome measurements including total hospital stay, in-hospital mortality, and intensive care unit (ICU) days were extracted for each cases. VAD was identified by using ICD-9 diagnostic code of 443.24. The presence of surgical and endovascular repairs in patients with VAD were identified by using ICD-9 procedure codes of (38.01, 38.02, 38.12, 38.31, 38.32, 38.41, 38.42, 38.62, 38.82, 39.56–39.59) and (00.55, 00.61, 00.62, 39.50, 39.72, 39.74, and 39.90) for surgical and endovascular procedures, respectively. Hospital outcome was quantified by identifying discharge to home, discharge to nursing facility, and in-hospital mortality.

Statistical Analysis

We compared the demographic and clinical characteristics, and the rate of in-hospital complications, ICU days, hospital length of stay, ventilator days, in-hospital mortality, and discharge destination between patients with VAD and those without VAD. Chi-square test and t test were used for categorical data and for continuous data, respectively with a p value <0.05 considered statistically significant.

Multivariate linear regression was performed to determine the effect of VAD on ICU days, hospital length of stay, and ventilator days after adjusting for age, gender, admission GCS score, and ISS. In the same fashion, multivariate logistic regression analysis was performed to identify the impact of VAD on in-hospital mortality and discharge destination after adjusting for the confounding factors. We used the SAS 9.3 software (SAS Institute, Cary, NC) for statistical analysis.

Results

A total of 684,632 patients were identified, who had been admitted with head and neck trauma and traumatic brain injury during the study period. Out of 684,623 patients, 84 patients had VAD which comprised 0.01 % of all patients with head and neck trauma. The mean age for patients with VAD was ~5 years higher than the mean age for patients without VAD [46 (95 % CI 41–50) vs. 41.3 (95 % CI 41.2–41.4); p = 0.003]. The patients with VAD had significantly lower admission GCS score with 31 % of them presenting with severe injury (GCS score <9) in comparison to 12 % in patients without VAD (p < 0.0001). The rate of cervical vertebral fracture was significantly higher in patients with VAD in comparison to patients without VAD [60 (71 %) vs. 74,110 (11 %); p < 0.0001]. The rates of obesity, cigarette smoking, and history of hypertension were not different among the two groups. Regarding the mechanism of injury, motor vehicle accident and fall were the most common causes resulting in 68 and 13 % of VADs, respectively. Firearm and cutting comprised 5 and 2 % of mechanism of injury in patients with VAD, respectively.

A total of 68 % of patients with VAD were treated in a university hospital, while the rate was 52 % for head and neck trauma patients without VAD (p = 0.003) (Table 1). The rate of in-hospital stroke was significantly higher in patients with VAD with 5 % of these patients experiencing stroke during hospital stay in comparison to 0.2 % of patients without VAD. Five patients had simultaneous carotid artery and VAD. None of the stroke events occurred in patients with concurrent carotid artery dissection. A total of 14 patients with VAD (17 %) had nosocomial pneumonia during hospital stay, which was significantly higher than the 3 % rate in patients without VAD (p < 0.0001). The mean hospital length of stay was 4 times higher in patients with VAD (22 vs. 5 days; p < 0.0001) (Table 1). The mean ICU days and ventilator days in patients with VAD were 7 and 8 days longer, respectively (p < 0.0001). The rate of in-hospital mortality was two-fold higher in patients with VAD, although the difference was not statistically significant (p = 0.07). The rate of discharge to home was significantly lower in patients with VAD (48 vs. 61 %, p = 0.015) and the rate of discharge to nursing facility was more than twice as high in these patients in comparison to patients without VAD (40 vs. 18 %, p < 0.0001).

Table 1 Baseline demographic and clinical characteristics, and hospital outcome of TBI and head and neck injury patients with and without vertebral artery dissection

The hospital length of stay remained significantly higher for patients with VAD after adjusting for age, gender, admission GCS score, and ISS [(OR: 6.7; 95 % CI 4.6–9.6); p < 0.0001]. The ICU days (OR: 3.8; 95 % CI 2.5–5.7) and the ventilator days (OR: 2.9; 95 % CI 1.7–5.0) remained significantly higher in patients with VAD after adjusting for age, gender, admission GCS score, and ISS. The odds of discharge to nursing facility remained significantly higher for patients with VAD after adjusting for age, gender, admission GCS score, and ISS (OR: 2.2; 95 % CI 1.4–3.5) (Table 2).

Table 2 Multivariate analysis determining the effect of vertebral artery dissection on various outcomes in patients with TBI and head and neck trauma

A total of six patients (7 %) with VAD underwent endovascular treatment. The mean (CI) ISS was significantly higher in patients who underwent endovascular procedures in comparison to the mean ISS in VAD patients without endovascular intervention [31 (21–40) vs. 17 (14–20), p = 0.014]. No incidence of in-hospital stroke was identified in patients who had endovascular intervention. None of the patients with VAD underwent surgical treatment of the VAD.

Discussion

In our analysis, diagnosed VAD was identified in 0.01 % of patients who were admitted with head and neck trauma. The first traumatic VAD was described by Suechting et al. [9]. in 1955 in a 29-year-old gentleman who developed a posterior inferior cerebellar artery infarction 18 h after a diving accident. Despite awareness of occurrence, the incidence of traumatic VAD is unknown as majority of the patients with vertebral artery injury initially remain asymptomatic [4, 10, 11]. It has been demonstrated that a symptom-free period of time ranging from 10 to 72 h may exist in patients with blunt VAD which makes early diagnosis more difficult [12]. Undiagnosed VAD may cause neurological deterioration with high morbidity and mortality secondary to distal thromboembolic events [13, 14]. Berne et al. [2] identified 0.09 % incidence rate for vertebral artery injury (including dissection and pseudo-aneurysm) in 3,480 patients with blunt injury to the common carotid artery or the extracranial or intracranial portion of the internal carotid artery or vertebral artery. Since, there was no systematic protocol for screening used in the NTDB, the incidence is an underestimate of actual incidence particularly in those with mild trauma. In single center studies, the rates of VAD in patients with blunt neck or head trauma range from 0.5 % in patients with blunt head and neck trauma to 50 % in patients with cervical spine fracture or dislocation, depending on the selection criteria to perform mandatory screening cerebral angiography [1519].

Occurrence or diagnosis of VAD was associated with higher rates of nosocomial pneumonia, longer hospital length of stay and ICU days, and higher chances of discharge to nursing facility. The initial severity of injury was greater among patients with VAD as assessed by ISS and GCS scores. Therefore, it is possible that higher rates of poor outcomes in these patients are secondary to greater severity of injury independent of VAD. However, the negative effect of VAD persisted after adjusting for age, gender, admission GCS score, and ISS. Our analysis cannot exclude the possibility that certain undetermined prognostic factors may have higher preponderance among patients with VAD. Some adverse outcomes may be a result of vertebrobasilar ischemic stroke secondary to thrombosis and/or occlusion or subarachnoid or intraparenchymal hemorrhage due to arterial bleeding [10, 13, 20].

The question remains whether an early diagnosis and treatment in patients with traumatic VAD could have reduced the mortality and resource allocation in these patients. The goal of treatment for patients with VAD is to prevent thrombosis, distal embolism, and compromise in regional cerebral blood flow [21]. The treatment of traumatic VAD can be challenging due to the risk of using anticoagulation or antiplatelet therapy in patients with multiple trauma. Medical treatment using anticoagulation and antiplatelet or thrombolytic agents is the first line of therapeutic strategy unless there are contraindications such as risk of bleeding or the intracranial extension of the dissection [22, 23]. In patients with persistent symptoms or extension of the dissection; or the development of dissecting aneurysm following medical therapy, surgical or endovascular interventions maybe considered [22, 24]. Endovascular treatment modalities such as coil embolization (internal trapping) and stent placement have shown promising long term clinical and angiographic results [2527]. Due to the lack of controlled multicenter clinical trials, the best treatment strategy and the value of aggressive treatment are yet to be described [28]. In our analysis, only 6 patients with VAD underwent endovascular treatment which includes 7 % of the patients with VAD. There was no incidence of stroke in patients who underwent endovascular treatment.

Our study has several limitations. As a retrospective study, we relied on the accuracy of primary ICD-9-CM diagnostic codes in hospitals records for identifying TBI patients and patients with head and neck trauma. Although ICD-9-CM diagnostic codes are frequently used to describe the epidemiology of TBI, different studies reported a variable sensitivity ranging from 61 to 89 % for these codes in identifying traumatic brain injury patients [13, 20]. To validate the methodology of ascertainment of arterial dissection using ICD-9 code (443.2, 443.21, and 443.24), Qureshi et al [29] compared the ICD-9-CM codes assigned to patients with ischemic stroke and dissection through reviewing medical record of ischemic stroke admissions at two university affiliated tertiary care hospitals in Minneapolis, MN. The positive predictive value was 82.1 % for the ICD-9-CM codes for dissection among 134 patients with ischemic stroke and dissection. Also, due to the retrospective nature of this study; we were unable to provide information about the diagnostic tests that were used to identify VAD and medical treatment administered in these patients.

Conclusion

Prospective clinical studies are required to identify the underlying mechanism for the role of VAD in increasing the rate of in-hospital mortality and resource allocation in patients with TBI and head and neck trauma. Furthermore, it remain to be determined whether a strategy focusing on early diagnosis and medical or endovascular treatment of VAD can reduce the rate of adverse outcomes in these patients.

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Acknowledgment

Dr. Majidi is supported by American Heart Association Clinical Research Program Award 13CRP17330020, Brain Edema at Cerebral Hemorrhage (BEACH) study. Dr. Qureshi is supported by National Institute of Neurological Diseases and Stroke. Principal Investigator, Antihypertensive Treatment in Acute Cerebral Hemorrhage (ATACH)-II. 1R01NS062091-01A2 (medication provided by EKR therapeutics) and American Heart Association Established Investigator Award 0840053N, Innovative Strategies for Treating Cerebral Hemorrhage.

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Majidi, S., Hassan, A.E., Adil, M.M. et al. Incidence and Outcome of Vertebral Artery Dissection in Trauma Setting: Analysis of National Trauma Data Base. Neurocrit Care 21, 253–258 (2014). https://doi.org/10.1007/s12028-013-9937-8

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Keywords

  • Vertebral artery dissection
  • Head trauma
  • Stroke
  • Endovascular treatment