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Eur J Cardiothorac Surg 2002;21:288-293
© 2002 Elsevier Science NL

Review

The mechanism of injury in blunt traumatic rupture of the aorta

^a Department of Cardiothoracic Surgery, Nottingham City Hospital, Hucknall Road, Nottingham NG5 1PB, UK
^b Transport Research Laboratory, Crowthorne, UK

Received 31 May 2001; received in revised form 2 November 2001; accepted 12 November 2001.

* Corresponding author. Tel.: +44-115-969-1169; fax: +44-115-840-2605
e-mail: drichens{at}ncht.trent.nhs.uk

	Abstract

Top Abstract 1. Introduction 2. Conditions for and... 3. The pathology and... 4. Future directions 5. Conclusions References

 
Rupture of the aorta accounts for a significant proportion of fatalities following blunt trauma. A great deal of consensus exists describing the circumstances under which acute traumatic aortic dissection occurs as well as its investigation and management. However, there remains some controversy surrounding the pathogenic aetiology underlying this injury. Univariate and multivariate models of blunt traumatic aortic rupture (BTAR) are discussed. To account for the consistency in the nature of BTAR, despite a range of trauma scenarios, the concepts of dynamic multivariate models and a final common pathway are introduced. Clinical management is described elsewhere. Greater understanding of the mechanism of BTAR could lead to a range of safety systems aimed at a reduction in its incidence and severity.

Key Words: Blunt trauma • Aortic rupture • Survival • Safety

	1. Introduction

Top Abstract 1. Introduction 2. Conditions for and... 3. The pathology and... 4. Future directions 5. Conclusions References

 
Disruption of the thoracic aorta following blunt trauma is commonly a catastrophic injury leading to death. As such it is identified in the advanced trauma life support (ATLS) franchise as one of eight ‘life-threatening chest injuries’ in the so-called ‘secondary survey’. The presentation, investigation and treatment of blunt traumatic aortic rupture (BTAR) are well described and commonly accepted in the literature [1–5]. However, there remains considerable uncertainty regarding the pathogenic aetiology of BTAR. The process is likely the result of both anatomic and mechanical factors. Some of the earliest investigators proposed that BTAR had a relatively simple univariate aetiology such as a sudden and dramatic rise in arterial blood pressure [6,7], while more contemporary theories propose that BTAR is a complex multivariate process secondary to combination of stresses [8,9]. Defining the process of BTAR may provide useful data for inclusion in the design of a range of safety systems. A reduction in the incidence and severity of BTAR could be expected to result in a lowering of mortality and morbidity far greater than that derived from more timely and accurate diagnosis and treatment. In addition, it may be speculated that addressing the safety requirements for prevention of BTAR would contribute to reducing the severity of other thoracic and abdominal injuries. This paper provides a review of the published literature describing the pathogenic aetiology of BTAR and suggests future direction for investigation. A discussion of the mechanisms of injury is included because this information is closely linked to the aetiology of BTAR.

	2. Conditions for and incidence of BTAR

Top Abstract 1. Introduction 2. Conditions for and... 3. The pathology and... 4. Future directions 5. Conclusions References

 
Recent studies suggest that in the USA and Canada around 7500–8000 victims die of BTAR every year [10]. By far, the largest percentage of patients diagnosed with BTAR have suffered automobile related trauma [1–4,10,11]. As a cause of death following automotive accident, BTAR (5–16%), [10,12] is second only to head injury (63%), [13,14]. Symbas [15] has concluded from the literature that one in every six to ten people killed in vehicular accidents sustain this injury. There is a consensus of opinion that BTAR is one of the leading causes of rapid death amongst automotive fatalities [3,16]. Dunn and Williams [17] quote a scene survival rate of 20% in patients with BTAR. Greendyke [11] determined from reviewing the published literature that the initial survival rate of BTAR is between 10 and 20%. One of the earliest reports to review the incidence and pathology of BTAR was presented by Parmley et al. [18]. In their combined autopsy and clinical review of 275 cases of BTAR it was reported that only thirty-eight managed to survive the initial insult, a survival rate of just 13.8%. It is further documented that of those surviving the initial insult, only two survived their injuries, the majority of the rest died within 15 days of the accident. Fabian et al. [10] reviewed 274 patients admitted to 50 trauma centres throughout North America and Canada. The authors found that of the 274 patients, 54 died directly as a result of BTAR. The total number of fatalities in this group was 86.

Although, as suggested BTAR principally results from automotive accidents, there are additional circumstances under which this injury occurs. Brundage et al. [19], report that a high proportion of pedestrian fatalities are a consequence of BTAR. Over a 6-year period in which 220 pedestrian fatalities were reported in King County (USA), 28 had BTAR (12.7%). The data reveals that 30 pedestrians were found to have BTAR with 24 of these dying at the scene. Of the remaining six who were taken to a treatment centre, only two survived their injuries. This leads to an overall mortality of 93.3% and a scene mortality of 80%. These figures are comparable with the mortality rates of BTAR resulting from automotive accidents. Mason [20] reports that the incidence of BTAR is also common amongst passengers involved in aircraft accidents. Its incidence in aircraft fatalities is as high as 43%, while Stevens [21], as cited by Mason [13], found the incidence of BTAR in light aircraft fatalities to be around 39%. Additional scenarios under which BTAR has occurred includes motorcyclists [10], victims involved in falls [1–3,10], an example in which an individual was struck by a falling tree [1,2] and one in which an individual was covered by silt during a cave-in [18].

As far as automotive accidents are concerned, studies have been performed to establish if there is any link between the type of vehicle impact and the initiation of BTAR. However, there are a number of conflicting variables that influence injury during a vehicle impact, many of which are difficult to quantify. This makes drawing any definitive relationships between vehicle impact and injury difficult. The variables that need to be considered include: vehicle design, position of the casualty in the car, speed and force of impact, behaviour of the vehicle after impact and whether safety systems were employed/deployed. Despite these confounding variables, some investigators have attempted to draw conclusions from impact scenarios and the incidence of BTAR. Arajarvi et al. [22] attempted to establish the relationship between seat belt use and the incidence of BTAR, through investigation of road accident data. They found in their sample of cases that unbelted occupants had proportionally more ruptures of the ascending aorta, while belted occupants tended to have a proportionally greater number of ruptures in the distal descending aorta. As for the ‘classical’ isthmus region where the aorta commonly ruptures, there was no proportional difference in the onset of this injury for either belted or unbelted occupants. The study also looked into the type of vehicle impact and demonstrated that ruptures can occur under a variety of scenarios, including frontal and lateral impacts. A similar study conducted by Shkrum et al. [23] also highlighted that significant numbers of BTAR fatalities occur under both frontal and lateral impacts. Arajarvi also found that rupture of the isthmus region of the aorta seemed to be equally frequent under both frontal and lateral vehicle impacts. It was also discovered that rupture of the distal descending aorta was frequently associated with fracture of the thoracic vertebra, which could be a contributory factor leading to BTAR of the aorta in this region. The effect of driver and passenger air bag systems on the incidence and severity of BTAR remains uncertain.

	3. The pathology and pathogenesis of BTAR

Top Abstract 1. Introduction 2. Conditions for and... 3. The pathology and... 4. Future directions 5. Conclusions References

 
It is clear that a number of potential factors may contribute to BTAR and it remains uncertain to what extent, if any, each plays a part and under what circumstances. Broadly speaking, anatomical and mechanical factors are important. The intention in this section is to discuss the pathology of BTAR and then its putative pathogenesis and the factors contributing to the aetiology of this disease.

3.1. Pathology of BTAR
BTAR typically involves a transverse tear in the wall of the aorta. The extent of the damage varies considerably between cases. In mild trauma, the injury may only be a partial circumferential tear in the intima, which may or may not extend into the medial layer of the aortic wall [16]. Under such circumstances, the intact adventitia may be strong enough to contain the circulation within the aorta and the individual stands a chance of survival [24]. Arterial blood pressure can force blood between the layers of the aortic wall forming a false aneurysm. If medical treatment is not initiated to treat the aneurysm it may eventually rupture, severely threatening the life of the individual. In more severe cases the tear can also extend into the adventitial layer, to the point where there is either a partial or complete transection of the aorta. Following a complete transection, blood exanguinates into the mediastinum and pleural cavity and the victim usually dies [24]. However, examples are presented in the published literature of individuals suffering a complete transection of the aorta, but managing to survive for a period adequate to allow medical intervention [18,25].

In contrast to the anatomical extent of the aorta, BTAR is limited to only a few specific locations along its length. It has been repeatedly referenced in the published literature that BTAR is most often confined to the descending aorta at the isthmus, often referenced as the ‘classical’ site of BTAR [3,16,24,26,27]. However, BTAR may occur in the ascending aorta proximal to the origin of the brachiocephalic artery. It is infrequent to find ruptures in the aortic arch, in the distal descending or abdominal aorta [3]. The majority of BTAR victims suffer a single rupture though there exist examples of multiple BTAR in a single individual [19]. For example, in the 21 individuals with multiple aortic ruptures reviewed by Moar [8], three were found to have up to eight tears in the aorta.

3.2. Pathogenesis of BTAR
Several different mechanical forces acting on the aorta, at anatomically susceptible sites, are important in BTAR (Fig. 1 ). The origin, transduction and relative importance of these forces remain uncertain and several different forces and hypotheses have been proposed over the years.

View larger version (22K): [in this window] [in a new window]   Fig. 1. Demonstration of the putative forces acting through the aorta during blunt traumatic injury (from Ref. [15]).

3.2.2. Intravascular pressure
Some early investigators attributed the occurrence of BTAR to a sudden rise in blood pressure [6,7,32]. However, this mode of failure of the aorta has been dismissed by a number of investigators, rationalising that if the aorta were an isotropic cylindrical vessel under pressure it would rupture axially rather than transversely. The typically observed transverse tears in the aorta could only occur if the transverse strength is more than twice the longitudinal strength. Tensile tests presented by Mohan and Melvin [30] and Yamada [31] do show that the ultimate tensile strength of the aorta in the transverse direction relative to the longitudinal direction does nearly approximate to the required rupture ratio of 2:1. Mohan and Melvin [30] demonstrated this point in bi-axial inflation tests conducted on aortic tissue samples. In the tests the aorta samples consistently failed transversely. Mohan and Melvin [30] also emphasised the point that the aorta is not a perfect cylinder and will deform during a vehicle impact. The forces acting through this altered aorta may be expected to dictate the nature of any subsequent tear. A number of investigators have conducted studies to establish the burst pressure for the aorta. Oppenheim [6] as cited by Klotz and Simpson [7], stated that the aorta bursts under a pressure of around 4.0x10⁵ N m^-2. However, Klotz and Simpson [7] found that inflating the aorta up to a pressure of 1.4x10⁵ N m^-2 did not produce a single rupture. However, Klotz and Simpson do state that as their analyses were conducted on aortic samples at post-mortem, the vessels may have suffered a change in their mechanical properties significant enough to influence their results. Furthermore, vessels in vivo are held in an initial state of pre-stress, which will not have been taken into account in the aortic inflation tests. Kroell et al. [33] investigated the increase in arterial pressure of the aorta during impacts to the chest. The aortas of complete cadavers were initially pressurised at baseline levels, after which the cadaver chests were impacted with different masses and travelling at various speeds. In their results, arterial pressures as high as 3.7x10⁵ N m^-2 were recorded. In two tests in which the aorta did rupture the pressures of the aorta were over 2.1x10⁵ N m^-2. These results suggest that the increase in arterial pressure during a vehicle impact may be significant enough to cause BTAR. The units quoted, admittedly give little indication of the clinical relevance of these forces. Zehnder (1956), as quoted by Kirlin and Barratt-Boyes [34], calculates that an intravascular pressure of around 2500 mmHg is required to produce rupture of the aorta.

3.2.3. Water-hammer effect
Lundewall [29] proposed that BTAR was the result of a ‘water-hammer’ effect. A water-hammer effect results when the flow of a non-compressible fluid is occluded dramatically, which leads to high-pressure waves being reflected back along the vessel wall. During vehicle impacts it is suspected that the aorta may be occluded at the point where it passes through the diaphragm as a result of the abdomen being compressed. The action of this hydrostatic response of the aorta has been studied with some simple analytical models [35,36]. In these investigations it was established that a sudden occlusion of the blood flow in the aorta would lead to a significant pressure pulse in the aorta. This would be expected to be significantly greater at the aortic arch on account of the curvature reflecting and intensifying the pressure wave. These analytical studies were unable to consider the additional deformation of the aorta during an impact where increasing the curvature of the aorta could possibly lead to greater increases in the pressure wave in this region.

3.2.4. Osseous pinch
A more novel mode of disruption of the aorta has been proposed by Crass et al. [37]. They hypothesise that the rupture of the aorta is due to an ‘osseous pinch’; entrapment of the aorta between the anterior thoracic bony structures (manubrium, first rib, medial clavicles and sternum) and the vertebral column. This hypothesis is based on a series of simple experiments conducted on physical models. A similar explanation was proposed by Symbas [3] who suggested that during high impacts to the sternum the aorta can be forced onto and stretched over the spine. However, the experiments of Crass et al. [37] neglected the influence that the presence of the other mediastinal structures would have on the response of the aorta during an impact to the chest.

3.2.5. Multivariate hypotheses
More contemporary theories propose that BTAR results from a combination of mechanisms including shear, torsion and stretching, compounded by hydrostatic forces [8]. Possible combined mechanisms leading to BTAR are described by Ben-Menachen and Handel [9]. During a vehicle impact in which the chest strikes the steering wheel Ben-Menachen and Handel [9] suggest that the compression force on the sternum and abdomen cause the mediastinum to displace upwards, often termed a ‘shovelling effect’. As the chest is compressed, the heart is squeezed between the sternum and the spine forcing blood from the heart into the aorta and creating a dramatic rise in the blood pressure of the aorta and pulmonary trunk. In addition, it is anticipated that at the level where the aorta passes through the diaphragm, it can kink and occlude the blood flow through the aorta and contribute to the rise in aortic blood pressure. This sudden occlusion of the blood flow can lead to high-pressure waves in the aorta due to a ‘water-hammer’ effect. The ‘shovelling effect’ displaces the heart and aortic arch upwards, while the descending aorta, which is tethered to the spine via the lungs remains fixed. The isthmus region of the descending aorta, which is at the junction between the fixed descending and upward displaced aortic arch, is placed under a torsional and tensile load. Being inherently weaker than the rest of the aorta the aorta tears at the isthmus. The increased pressure in the aorta adds to the loading of the aorta at the isthmus. Ben-Menachen and Handel further hypothesise that the part played by the ligamentum arteriosum in tearing the aorta is limited. The ‘shovelling effect’ displaces all of the mobile mediastinal organs and vessels including the heart, aortic arch and the pulmonary vessels. Consequently, there is no stretching of the ligamentum arteriosum, which is also evident from the limited number of injuries to the pulmonary trunk.

As proposed in the work of Gotzen et al. [38] the direction of the impact to the chest and the resulting deformation of the thorax are significant to the type of mechanisms that contribute to aortic rupture. From analysing cases of aortic rupture they proposed that impact to the chest acting from right ventro-caudal to left dorso-caudal predominated. They surmised that this type of impact would force the heart and aortic arch upwards posteriorly and to the left, leading to stretching and shearing of the aorta at the isthmus. They found that BTAR at the isthmus was not as common if the impact was directed from left ventro-caudal to right dorso-caudal. It is additionally suggested that during this type of impact rupture may even be prevented by the limited movement of the mediastinal organs against the spinal column.

3.3. Additional factors in the pathogenesis of BTAR
It has been speculated that under a specific set of conditions certain groups of the population may be more susceptible than others to BTAR. The strength of arterial vessels including the aorta is known to weaken with disease, such as cystic medionecrosis and syphilis. These may contribute to the initiation of the injury if present within an individual, but as discussed by Shkrum et al. [23], they are not a pre-condition to the occurrence of BTAR. A more common factor is that age has a detrimental affect on the mechanical properties of the aorta through arteriosclerosis, reducing the ultimate tensile strength and strain of the vessel [30,31]. Again, although this may contribute to the onset of the injury there is no evidence to suggest that it is a pre-condition of the injury, as the injury has been shown to occur in significant numbers in all age ranges.

	4. Future directions

Top Abstract 1. Introduction 2. Conditions for and... 3. The pathology and... 4. Future directions 5. Conclusions References

 
The literature reveals a number of conflicting, unsubstantiated hypotheses that provide plausible explanations for the mechanism of BTAR. Historically, simple models were considered based on the behaviour of the aorta in isolation. This possibly explains why some investigators have tended to idealise a single mechanism as being responsible for BTAR. This is certainly the case with the hypotheses suggesting stretching, intravascular pressure and osseous pinch, as single mechanisms accounting for BTAR. Subsequently, more complex multifactorial systems were considered. Theories explaining BTAR as a consequence of a multitude of mechanisms do tend to consider the complete dynamics of the thorax and its internal structures during an impact. There are at least two areas that remain under investigated. Firstly, the concept of the final common pathway to account for the observation that a multitude of different traumas result in a limited number of forms of BTAR. Secondly, the inclusion of the cardiopulmonary cycle into multifactorial models to account for the entire range of forces acting on the aorta at any given moment.

4.1. The final common pathway
In contrast to blunt trauma to the abdomen where the resulting injuries are varied and unpredictable, blunt trauma to the thorax leads to relatively specific, and in the case of the aorta, predictable injuries. However, the nature of these forces and their transduction remains elusive. Previous authors discussing BTAR have surmised that the primary initiator of the injury is either high-deceleration loads or a result of crushing of the aorta [16,27]. However, considering the accident scenarios under which BTAR occurs and deciding how it is possible to differentiate whether BTAR is the result of a deceleration, acceleration or a crushing load is difficult. Many authors have stated that BTAR arising from falls is generally the result of high decelerations. However, the deceleration response will inevitably bring about a deformation in the spine and thoracic cage due to their flexibility, whether this be hyper-extension, flexion or lateral flexion. This response will in itself apply a crushing mechanical load on the organs within the thorax. Only if the thoracic cage was a purely rigid system would the loading on the internal organs be a purely deceleration load. Alternatively, slow compression of the chest (similar to the effect of a mechanical press) would apply a pure crushing load, but no cases are given in which aortic rupture arose under these precise conditions. It is acceptable that the thorax is crushed during vehicle impacts, but the crushing response will also apply a deceleration pulse on the body. Based on this rationalisation, it seems to suggest that BTAR arises under conditions of both crushing and deceleration/acceleration, though it is not possible, based on available data, to determine which of these is the primary mechanism for BTAR. Symbas [15] has concluded that torsion stress and stress from the water-hammer effect are more likely to affect the ascending aorta, while shearing and bending stresses are likely responsible for rupture of the aorta at the isthmus (Fig. 1). Deceleration, acceleration and crush forces acting through a multitude of vectors and conditions result in a limited number of aortic injuries. A key question remains, how are these energies transduced through the thorax to susceptible sites causing BTAR. It seems reasonable to conclude that there is ‘final common pathway’ through which BTAR is initiated. This may be expected to take the form of either anatomical or mechanical variables, but is more likely a combination of both acting in a given time frame. Defining the point of convergence of a number of different mechanisms that elicit BTAR would be key to understanding why this injury is so consistent in its nature. One may expect more efficient safety systems if the point of convergence is relatively ‘upstream’ in the disease aetiology.

4.2. Dynamic multivariate models
The literature supports the view that in order to understand the mechanisms that are responsible for BTAR, the haemodynamics and pulmonary dynamics of the chest need to be understood. It has been speculated that the occurrence and severity of BTAR could be dependent on the phase of the heart and lungs during the insult. As cited by Kivity and Collins [36], McDonald and Campbell [39] highlighted that the injury could be more likely at the start of diastole when the aorta is full of blood and at its maximum state of loading. In addition, the lungs in a state of full inspiration could potentially provide additional cushioning or conversely greater loading on the aorta during impacts to the chest.

Consequently, any model developed to investigate BTAR should be able to consider all plausible mechanisms that potentially cause BTAR before any significant conclusions can be drawn about the mechanisms responsible for the injury. Future work in this area needs the creation of an inclusive, dynamic model with data from haemodynamics, pulmonary dynamics and structural dynamics. Given the number of variables and computations in a dynamic system, it is reasonable to conclude the future lay in computer based modelling systems

	5. Conclusions

Top Abstract 1. Introduction 2. Conditions for and... 3. The pathology and... 4. Future directions 5. Conclusions References

 
Although referenced as a common cause of death in the published literature, it was found that there are still no definitive answers as to what the fundamental mechanisms are that cause this injury, though a great deal of speculation exists on what these might be. The high level of reproducibility of the site and nature of blunt traumatic rupture intuitively suggests that there is a reproducible mechanism of injury. Early investigators supported the view that the injury resulted from one specific mechanical loading: from either stretching of the aorta, shearing due to deceleration loads, increases in internal blood pressure or pinching of the aorta between the osseous bodies of the chest. Current thinking proposes that the injury results from a number of mechanical factors which all contribute to the onset of the injury. Future work in this area needs the creation of an inclusive, dynamic model. Given the number of variables and computations in a dynamic system, it is reasonable to conclude the future lay in computer based modelling systems. Greater understanding of the mechanism of injury could lead to improved vehicle safety leading to a reduction in its incidence and severity.

	References

Top Abstract 1. Introduction 2. Conditions for and... 3. The pathology and... 4. Future directions 5. Conclusions References

 

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