전체메뉴
Article Search

VSI Vascular Specialist International

Open Access

pISSN 2288-7970
eISSN 2288-7989
QR Code QR Code

Review

Article

Review

Vascular Specialist International 2016; 32(1): 1-5

Published online March 31, 2016 https://doi.org/10.5758/vsi.2016.32.1.1

Copyright © The Korean Society for Vascular Surgery.

Traumatic Carotid Artery Dissection: A Different Entity without Specific Guidelines

George Galyfos1, Konstantinos Filis1, Fragiska Sigala1, and Argiri Sianou2

1Vascular Division, First Propedeutic Department of Surgery, Hippocration Hospital, Athens, Greece, 2Department of Microbiology, Areteion University Hospital, Athens, Greece

Correspondence to:George Galyfos, Vascular Division, First Propedeutic Department of Surgery, Hippocration Hospital, 6 Melinas Merkouri Street, Neon Irakleion, Attikis, 14122 Athens, Greece Tel: 30-6938764167, Fax: 30-2132086455, E-mail: georgegalyfos@hotmail.com

Received: February 23, 2016; Accepted: March 11, 2016

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

According to literature data, there are no distinct guidelines regarding the proper diagnostic and therapeutic management of traumatic carotid artery dissection (TCAD). Although most of cases evaluated in research studies refer to spontaneous carotid artery dissection, traumatic cases demand special considerations as far as diagnosis and treatment are concerned. Although both types of dissection share some common characteristics, a patient with TCAD usually presents with several concomitant injuries as well as a higher bleeding risk, thus complicating decision making in such patients. Therefore, aim of this review is to present available data regarding epidemiology, clinical presentation, diagnostics and treatment strategy in cases with TCAD in order to produce useful conclusions for everyday clinical practice.

Keywords: Carotid arteries, Nonpenetrating wounds, Anticoagulation, Endovascular

INTRODUCTION

Traumatic carotid artery dissection (TCAD) is a different clinical entity compared to spontaneous carotid dissection demanding special considerations regarding proper management.

Recent guidelines on carotid disease management do not make any differentiation among spontaneous and traumatic dissection [1]. According to these guidelines, antithrombotic or antiplatelet treatment is recommended in patients with neurological symptoms (Class IIa, Level B recommendation) and endovascular intervention is suggested only when neurological status of a patient deteriorates under conservative medical treatment (Class IIb, Level C recommendation) [1]. However, considering traumatic cases, special issues should be taken under consideration.

Therefore, this review aims to highlight the specific characteristics of epidemiology, clinical presentation, diagnostic investigation and proper treatment in patients with traumatic dissection of the carotid artery.

EPIDEMIOLOGY

In general, blunt carotid injury is observed in 1%–2.6% of blunt trauma cases and in 2.7% of patients with severe multisystem trauma [2]. Moreover, blunt carotid injury has been associated with a high stroke rate (up to 60%) and mortality rate (19%–43%) [3]. Many of these cases are asymptomatic and they remain undetected until symptoms of cerebrovascular ischemia present. Recent data indicate that symptoms occur after a mean of 12.5 hours in survivors, and after a mean of 19.5 hours in non-survivors [3]. However, TCAD is very rare (estimated incidence 0.08%), and although it is associated with mild symptoms, it can sometimes be fatal [4]. Thus, this type of dissections is often overlooked life-threatening injuries. Even though most of the carotid artery dissections occur spontaneously, about 4% of the dissections are related to severe trauma. Furthermore, spontaneous dissections are usually seen in older patients (over 50 years of age) although traumatic dissections mostly affect young patients around 40 years of age [5].

Regarding the mechanism of injury, TCAD may result from a direct blow to anterolateral aspect of the neck, or an extreme extension and rotation of the neck. Trauma mechanisms involved are variable, ranging from high speed motor vehicle accidents to trivial traumas in certain groups of patients (for example patients with hypertension or connective tissue diseases). Distraction/extension, distraction/flexion or lateral flexion forces of the cervical spine may result in traumatic TCADs as well [5]. Even a vasocompression between C-spine and mandibula during a hyperinclination trauma can lead to a dissection of the internal carotid artery. The forces implicated in such injuries may cause small lesions of the vessel wall, which could result in intimal tears, intramural hematomas or complete lumen displacement/obstruction [6].

Although there are certain vascular risk factors associated to spontaneous dissection such as coronary heart disease (33%), hypertension (57%), and hypercholesterolemia (29%), history of smoking (45%) and history of migraine (21%), in younger patients suffered from TCAD the aforementioned factors are usually not present [7]. Moreover, in cases of spontaneous dissections, no history of any kind of cervical trauma or stressful movement is reported. Intrinsic susceptibiliity has been observed in certain patients with monogenic connective tissue disease (Ehlers Danlos syndrome, Marfan syndrome, polycystic kidney disease, deficiency of alpha-1 antitrypsin and hereditary hemochromatosis). Almost 2% of dissections have been correlated with such conditions [7].

CLINICAL PRESENTATION

Only 10% of cases present immediate symptoms although most clinical signs usually occur within the first 24 hours of the occurrence of the trauma. TCAD is suspected and diagnosed when neurological symptoms occur unexpectedly after a trauma of the neck or the head. The most frequent presentations of TCAD are stroke, Hörner syndrome due to pressure of a hematoma, and paralysis of a cranial nerve. TCAD evolves into stroke in 80% of cases within the first week of the trauma. The common cause of stroke is arterial thrombosis resulting in permanent neurological deficits, with a mortality rate approaching 40% [8]. Due to the traumatic mechanism, bleeding through the oral cavity, nostrils or ears could be detected as well. Time of ischemic signs onset is very variable too, diverging from immediate to several months delay [9].

Unlike spontaneous cases, these patients present with concomitant injuries of the neck or the skull, and frequently, their cognitive status is significantly altered. Almost one third of such patients could present with a cerebrovascular infarct that could not be justified otherwise. Therefore, several risk indices (Denver group criteria, Memphis or Kerwin criteria) have been developed in order to early screen such patients and proceed with proper treatment promptly [10]. Such indices share most of their included risk factors such as neurologic status incosistent with radiologic findings, severe soft tissue injury/hematoma of the neck, high grade facial fractures and high risk mechanism of injury (Fig. 1). Biffl et al. [11] have added and some other factors such as Glascow coma scale <6 and diffuse axonal injury. Hence, the number of risk factors present is strongly associated with increasing stroke and mortality risk as well. Such criteria are essential for early screening in order to identify patients in higher risk for blunt carotid injuries yielding a high sensitivity and specificity. Additionally, the cost of long-term rehabilitation care and human life after dissection-associated neurologic events is substantial [12]. Therefore, prompt identification of such patients is imperative in order to proceed with further imaging investigation and proper treatment [13].

DIAGNOSTIC INVESTIGATION

Duplex ultrasonography has the advantage of being a non-invasive method although its performance is strongly affected by the experience of the operator. Furthermore, this modality shows a high disposability even in smaller rural hospitals, making it the first choice for most practitioners as far as early screening is concerned. It is a common method to detect a possible vascular injury, although it offers a poor vision of the intracranial aspects of a TCAD and it also gives limited information about small intimal tears [6]. Finally, when extensive soft tissue injuries present, the sensitivity of diagnostic ultrasound is even lower in case of traumatic dissections compared to spontaneous cases.

Although, the golden standard for identifying a possible dissection is digital subtraction angiography (DSA) according to many authors [3], computed tomography angiography (CTA) would probably be more appropriate as initial screening modality in cases of severe trauma. DSA offers a very high diagnostic performance of 97% for vascular injuries and at the same time, it permits a potential intervention via endovascular techniques when indicated (Fig. 2) [11]. However, DSA is an invasive method with a complication rate of almost 1%, and it is not readily available in all institutions, especially in those without an endovascular suite. However, computed tomography (CT) scan combined with CTA would be more appropriate in identifying carotid dissections in patients with severe trauma as it would facilitate the detection of concomitant cerebral or vertebral injuries [14]. “String signs”, indicating constrictions of the lumen, are reckoned to be indirect signs of artery dissection. Moreover, recent data indicate that traumatic dissections present higher (Segment III; level of first-second cervical vertebrae) compared to spontaneous dissections (Segment I; origin of vessel up to fifth cervical vertebrae) [15]. According to Harrigan et al. [16], CTA was selected in almost 60% of cases in a large series of more than 11,000 patients with blunt cervical trauma. Hence, a recent evaluation of CTA with 16-section CT scanners has demonstrated 97.7% sensitivity and 100% specificity compared with the criterion standard of conventional DSA [17]. Therefore, many authors suggest CTA in such patients followed by DSA for inconclusive cases or when endovascular repair is indicated.

Finally, magnetic resonance (MR) scanning combined with MR angiography (MRA) could be an alternative for early TCAD detection. Especially for blunt trauma, MRA determines dissections in up to 99% and provides additional information about concomitant injuries such as brain injuries or skull fractures [3,18]. Recent data show that MRA is equal to CTA in the diagnosis of carotid and vertebral artery dissection in general [18]. However, there are specific concerns for TCAD cases. First of all, MRA is not available in all institutions as an emergency modality, especially in smaller hospitals. Additionally, besides the long duration of the scan, the existance of metal objects or life supporting devices (fragments, implants, pacemakers etc.) within the trauma or the upper body of the patient would raise contraindications for undergoing such investigation.

TREATMENT

In general, asymptomatic patients with low-grade dissections are typically treated conservatively with medical management and close imaging observation [19]. The majority of these cases achieve anatomic and symptomatic resolution, with low rates of recurrence over long-term follow-up [20]. Regarding proper medical treatment for spontaneous carotid artery dissection, anticoagulation or antiplatelets should be initiated promptly to prevent further thromboembolic events [1,5,6]. Data so far indicate that both type of agents show similar efficacy in reducing neurological sequalae without increasing the risk for stroke [19,21]. However, cases of traumatic causes demand a more interdisciplinary approach and show specific considerations concerning treatment.

When other concomitant injuries with a high risk for severe bleeding are present (for example major fractures of long bones or pelvis, solid organ injuries within the abdomen or the thorax, closed head injuries etc.), then the optimal type and time of treatment should be considered in an interdisciplinary approach (including consultation by a trauma surgeon, orthopedic surgeon, neurosurgeon, vascular surgeon, radiologist, neurologist). For most of cases, medical treatment should be initiated as soon as possible. When anticoagulants are initiated, the therapeutic heparinization should be regulated according to partial thromboplastin time levels (50–70 seconds), followed by per os treatment (international normalized ratio 2–3) for at least 3 months. However, practitioners should always take into consideration the patient’s risks, comorbidities and overall injuries when deciding on the proper agent. According to some authors, anticoagulation is preferred to antiplatelet agents in cases of severe stenosis, arterial occlusion or pseudoaneurysm although antiplatelets are preferred when high risk for bleeding, inadequate collateral circulation or large infarcts are present [6]. Finally, concerning the role of thrombolysis in TCAD, data are limited in literature given the high bleeding risk in trauma patients. Even for spontaneous dissection, the results seem to be contradictory [22].

Regarding the role of endovascular treatment for TCAD, this minimally invasive method is becoming more popular lately, and it is described as a good therapeutic alternative even for traumatic cases [23], although there have been reports of high complication and occlusion rates with high grade injuries in the past [24]. In a recent meta-analysis on endovascular management of carotid dissections, the method has shown optimal technical success, low recurrent rates and satisfying one year follow-up. Hence, one third of the included patients were traumatic cases [25]. In this review, the authors suggest the following criteria for stenting: (i) patients with recurrent symptoms despite medical therapy, (ii) patients with hemodynamic hypoperfusion (involvement of multiple vessels or poor collateral vessels), (iii) patients with expanding or symptomatic pseudoaneurysm and (iv) contraindication to anticoagulation because of intra-cranial or systemic hemorrhage [25]. Furthermore, in a more recent study by Spanos et al. [26], overall 193 patients were treated endovascularly for TCAD yielding low periprocedural morbidity and mortality rates, namely 6% and 1.2% respectively, as well as low re-intervention rate during long-term follow-up.

Finally, endovascular repair with stenting also requires pre- and post-treatment antiplatelet therapy to avoid embolic complications or stent occlusion. In the aforementioned study, antiplatelet therapy (either single or dual) was initiated postoperatively, lasting from three months to inevitably with good longterm outcomes [26]. However, this often results in a frustrating clinical conundrum because many patients are referred for endovascular repair specifically due to contraindications to antithrombotic therapy such as severe intracranial injury, multisystem trauma, or penetrating injuries. Seth et al. [2] suggest avoiding the placement of stents in patients who have not or are not able to receive appropriate pre- and post-procedural antiplatelet therapy, unless faced with an immediately life-threatening injury.

CONCLUSION

Patients with TCAD remain a subgroup of cases that require special considerations and management in an interdisciplinary setting. Although presenting not frequently and with a subtle clinical picture at the beginning, this entity is associated with major morbidity and mortality. Thus, guidelines for proper detection and treatment need to be adjusted in order to achieve optimal results.

Fig 1.

Figure 1.Trauma patient with soft tissue injury of the neck and altered mental status due to traumatic carotid artery dissection. The patient was intubated due to low Glascow scale.
Vascular Specialist International 2016; 32: 1-5https://doi.org/10.5758/vsi.2016.32.1.1

Fig 2.

Figure 2.Digital subtraction angiography illustrating a traumatic dissection of the common carotid artery (arrow) and an occlusion of the internal carotid artery.
Vascular Specialist International 2016; 32: 1-5https://doi.org/10.5758/vsi.2016.32.1.1

References

  1. Brott, TG, Halperin, JL, Abbara, S, Bacharach, JM, Barr, JD, and Bush, RL (2011). 2011 ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the management of patients with extracranial carotid and vertebral artery disease: executive summary. Circulation. 124, 489-532.
    Pubmed CrossRef
  2. Seth, R, Obuchowski, AM, and Zoarski, GH (2013). Endovascular repair of traumatic cervical internal carotid artery injuries: a safe and effective treatment option. AJNR Am J Neuroradiol. 34, 1219-1226.
    CrossRef
  3. Lee, TS, Ducic, Y, Gordin, E, and Stroman, D (2014). Management of carotid artery trauma. Craniomaxillofac Trauma Reconstr. 7, 175-189.
    Pubmed KoreaMed CrossRef
  4. Davis, JW, Holbrook, TL, Hoyt, DB, Mackersie, RC, Field, TO, and Shackford, SR (1990). Blunt carotid artery dissection: incidence, associated injuries, screening, and treatment. J Trauma. 30, 1514-1517.
    Pubmed CrossRef
  5. Cr?nlein, M, Sandmann, GH, Beirer, M, Wunderlich, S, Biberthaler, P, and Huber-Wagner, S (2015). Traumatic bilateral carotid artery dissection following severe blunt trauma: a case report on the difficulties in diagnosis and therapy of an often overlooked life-threatening injury. Eur J Med Res. 20, 62.
    Pubmed KoreaMed CrossRef
  6. Mohan, IV (2014). Current optimal assessment and management of carotid and vertebral spontaneous and traumatic dissection. Angiology. 65, 274-283.
    CrossRef
  7. Thomas, LC, Rivett, DA, Attia, JR, and Levi, CR (2012). Risk factors and clinical presentation of craniocervical arterial dissection: a prospective study. BMC Musculoskelet Disord. 13, 164.
    Pubmed KoreaMed CrossRef
  8. Bayır, A, Aydo?du Kıre?i, D, S?ylemez, A, and Demirci, O (2012). Cerebral infarction caused by traumatic carotid artery dissection. Ulus Travma Acil Cerrahi Derg. 18, 347-350.
    CrossRef
  9. Makhlouf, F, Scolan, V, Detante, O, Barret, L, and Paysant, F (2013). Post-traumatic dissection of the internal carotid artery associated with ipsilateral facial nerve paralysis: diagnostic and forensic issues. J Forensic Leg Med. 20, 867-869.
    Pubmed CrossRef
  10. Martinakis, VG, Dalainas, I, Katsikas, VC, and Xiromeritis, K (2013). Endovascular treatment of carotid injury. Eur Rev Med Pharmacol Sci. 17, 673-688.
    Pubmed
  11. Biffl, WL, Cothren, CC, Moore, EE, Kozar, R, Cocanour, C, and Davis, JW (2009). Western Trauma Association critical decisions in trauma: screening for and treatment of blunt cerebrovascular injuries. J Trauma. 67, 1150-1153.
    Pubmed CrossRef
  12. Cothren, CC, Moore, EE, Ray, CE, Ciesla, DJ, Johnson, JL, and Moore, JB (2005). Screening for blunt cerebrovascular injuries is cost-effective. Am J Surg. 190, 845-849.
    Pubmed CrossRef
  13. Miller, PR, Fabian, TC, Croce, MA, Cagiannos, C, Williams, JS, and Vang, M (2002). Prospective screening for blunt cerebrovascular injuries: analysis of diagnostic modalities and outcomes. Ann Surg. 236, 386-393.
    Pubmed KoreaMed CrossRef
  14. Ofer, A, Nitecki, SS, Braun, J, Daitzchman, M, Goldsher, D, and Hoffman, A (2001). CT angiography of the carotid arteries in trauma to the neck. Eur J Vasc Endovasc Surg. 21, 401-407.
    Pubmed CrossRef
  15. Lleva, P, Ahluwalia, BS, Marks, S, Sahni, R, Tenner, M, and Risucci, DA (2012). Traumatic and spontaneous carotid and vertebral artery dissection in a level 1 trauma center. J Clin Neurosci. 19, 1112-1114.
    Pubmed CrossRef
  16. Harrigan, MR, Weinberg, JA, Peaks, YS, Taylor, SM, Cava, LP, and Richman, J (2011). Management of blunt extracranial traumatic cerebrovascular injury: a multidisciplinary survey of current practice. World J Emerg Surg. 6, 11.
    Pubmed KoreaMed CrossRef
  17. Eastman, AL, Chason, DP, Perez, CL, McAnulty, AL, and Minei, JP (2006). Computed tomographic angiography for the diagnosis of blunt cervical vascular injury: is it ready for primetime?. J Trauma. 60, 925-929.
    Pubmed CrossRef
  18. Provenzale, JM, and Sarikaya, B (2009). Comparison of test performance characteristics of MRI, MR angiography, and CT angiography in the diagnosis of carotid and vertebral artery dissection: a review of the medical literature. AJR Am J Roentgenol. 193, 1167-1174.
    Pubmed CrossRef
  19. Cothren, CC, Moore, EE, Biffl, WL, Ciesla, DJ, Ray, CE, and Johnson, JL (2004). Anticoagulation is the gold standard therapy for blunt carotid injuries to reduce stroke rate. Arch Surg. 139, 540-545.
    Pubmed CrossRef
  20. Rao, AS, Makaroun, MS, Marone, LK, Cho, JS, Rhee, R, and Chaer, RA (2011). Long-term outcomes of internal carotid artery dissection. J Vasc Surg. 54, 370-374.
    Pubmed CrossRef
  21. Cothren, CC, Biffl, WL, Moore, EE, Kashuk, JL, and Johnson, JL (2009). Treatment for blunt cerebrovascular injuries: equivalence of anticoagulation and antiplatelet agents. Arch Surg. 144, 685-690.
    Pubmed CrossRef
  22. Zinkstok, SM, Vergouwen, MD, Engelter, ST, Lyrer, PA, Bonati, LH, and Arnold, M (2011). Safety and functional outcome of thrombolysis in dissection-related ischemic stroke: a meta-analysis of individual patient data. Stroke. 42, 2515-2520.
    Pubmed CrossRef
  23. Patel, RR, Adam, R, Maldjian, C, Lincoln, CM, Yuen, A, and Arneja, A (2012). Cervical carotid artery dissection: current review of diagnosis and treatment. Cardiol Rev. 20, 145-152.
    Pubmed CrossRef
  24. Cothren, CC, Moore, EE, Ray, CE, Ciesla, DJ, Johnson, JL, and Moore, JB (2005). Carotid artery stents for blunt cerebrovascular injury: risks exceed benefits. Arch Surg. 140, 480-485.
    Pubmed CrossRef
  25. Xianjun, H, and Zhiming, Z (2013). A systematic review of endovascular management of internal carotid artery dissections. Interv Neurol. 1, 164-170.
    CrossRef
  26. Spanos, K, Karathanos, C, Stamoulis, K, and Giannoukas, AD (2016). Endovascular treatment of traumatic internal carotid artery pseudoaneurysm. Injury. 47, 307-312.
    CrossRef