Forensic Science International 236 (2014) e1–e4
Contents lists available at ScienceDirect
Forensic Science International journal homepage: www.elsevier.com/locate/forsciint
Case Report
Bilateral middle cerebral artery infarction associated with traumatic common carotid artery dissection: A case report and review of literature Fumiko Chiba a,*, Yohsuke Makino a,b, Ayumi Motomura a, Go Inokuchi a, Namiko Ishii a, Suguru Torimitsu a, Ayaka Sakuma a, Sayaka Nagasawa a, Hisako Saito a, Daisuke Yajima a, Mutsumi Hayakawa a, Hirotaro Iwase a a b
Department of Legal Medicine, Graduate School of Medicine, Chiba University, Inohana 1-8-1, Chuo-ku, Chiba City, Chiba Prefecture 260-8670, Japan Department of Radiology, Graduate School of Medicine, Chiba University, Inohana 1-8-1, Chuo-ku, Chiba City, Chiba Prefecture 260-8670, Japan
A R T I C L E I N F O
A B S T R A C T
Article history: Received 20 June 2013 Received in revised form 26 December 2013 Accepted 3 January 2014 Available online 10 January 2014
Traumatic common carotid artery dissection is very rare, and although it is associated with mild symptoms, it can sometimes be fatal. Therefore, careful examination of common carotid artery dissection and additional pathological examination as appropriate are important during the autopsy of traumatic death patients. A 60-year-old previously healthy drunken woman was run over. She had remained unconscious shortly after the accident, and 15 h later, emerging bilateral cerebral infarction was confirmed using brain computed tomography. Despite conservative management, she died 4 days after the injury due to multiple chest traumas and broad cerebral infarction. A medico-legal autopsy was conducted. According to the autopsy results, microscopically identified common carotid artery dissections with thrombus formation were considered the cause of infarction. In the present case, macroscopic common carotid artery lesions were relatively mild, and this made diagnosis difficult. However, the correct diagnosis was achieved by a combined analysis of the antemortem images and autopsy results. Thus, in such cases, a combined comprehensive analysis of autopsy results and antemortem clinical images is important to determine the exact cause of death. ß 2014 Elsevier Ireland Ltd. All rights reserved.
Keywords: Traumatic common carotid artery dissection Middle cerebral artery Cerebral infarction Antemortem images Forensic pathology
1. Introduction In general, common carotid artery dissection (CCAD) represents a complication of aortic dissection, and traumatic CCAD is very rare. To the best of our knowledge, only 17 articles (Table 1), including ours, on traumatic CCAD have been reported thus far in the English literature [1–11]. In addition, only one study thus far reported their findings by in-depth examination of autopsy results [11]. In this study, we describe the second autopsy case of traumatic CCAD associated with fatal cerebral infarction. 2. Case report A 60-year-old previously healthy drunken woman lying on the road was run over by a mini-vehicle. Her blood pressure was normal and spontaneous breathing was sustained. Her electrocardiogram showed a normal sinus rhythm, but she was unconscious
* Corresponding author. Tel.: +81 43 226 2078; fax: +81 43 226 2079. E-mail address: [email protected] (F. Chiba). 0379-0738/$ – see front matter ß 2014 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.forsciint.2014.01.003
when the emergency services arrived. She was brought to the hospital 30 min after the accident. She remained unconscious and was thus placed on ventilator support. Her blood level of ethanol was 286.2 mg/dL. A computed tomography scan was performed with a 128-row detector CT (Siemens Somatom Definition AS, Siemens Medical Systems, Forchheim, Germany) and the scanning protocol was as follows: tube voltage 120 kV; automatically regulated tube current: about 100–400 mA; pitch 0.8; collimation of 4.8–9.6 mm; rotation time 0.5 r/sec. DICOM image reconstruction protocol was as follows: image matrix, 525 525; slice thickness of 10 mm; field of view, 336 mm 336 mm; reconstruction kernel, B41f. A head CT taken 1 h after the accident revealed sporadic, slightly low-dense areas in both cerebral cortices (Fig. 1). Contrast-enhanced thoracoabdominal CT revealed asymmetrically thickened walls in both the common carotid arteries, and carotid artery dissection was suspected (Fig. 2). Given her general status, she was not a candidate for surgery and conservative management was begun. Head CT was performed 15 h after the injury with a 320-row detector CT (Aquilion ONE, Toshiba Medical Systems, Nasu, Japan) and the scanning protocol was as follows: tube voltage 120 kV; automatically regulated tube current: about
F. Chiba et al. / Forensic Science International 236 (2014) e1–e4
e2
Table 1 Literature review of common carotid artery dissection. Age (years), sex
Cause
Side
Clinical symptoms
Outcome
Citation
68, 37, 33, 30, 42, 58, 41, 42, 19, 50, 20, 61, 27, 43, 38, 42, 60,
Blunt neck injury Blunt neck injury Hanging injury Motor vehicle accident Motor vehicle accident Fall with neck trauma Hanging injury Blunt neck injury Motor vehicle accident Hanging injury Blunt neck injury Strangulation Blunt neck injury Motor vehicle accident Manual strangulation Manual strangulation Motor vehicle accident
Right Left Left and Right Right Right Right Right Right Right Right Left and Left Left Left and Left and Left and
Left hemiparesis, unilateral spatial neglect Neck pain Left hemiparesis Tetraplegia Left hemiparesis Left hemiparesis Dizziness Left hemiparesis, DOC (GCS score, not available) Visual loss Left upper limb weakness Left hemiparesis Tetraplegia, left hemiparesis Right hemiparesis, aphasia Difficulty finding words Right hemiparesis, DOC (GCS, 9), bilateral Babinski Headache Disturbance of consciousness (GCS, 3)
Alive Alive Alive Alive Alive Alive Alive Alive Alive Alive Dead Alive Alive Alive Dead Alive Dead
[1] [2] [3] [4] [4] [4] [4] [4] [5] [6] [7] [8] [9] [10] [11] [11] Current report
male male female female female female female male female female male female male female male female female
right
right
right right right
400 mA; pitch 0.813; collimation of 0.5 mm; rotation time 0.5 r/s. DICOM image reconstruction protocol was as follows: image matrix, 525 525; slice thickness of 10 mm; field of view, 345.1 mm 345.1 mm; reconstruction kernel, FC04. The head CT revealed broad enlarged low-density areas in both the hemispheres (Fig. 3). The distribution of low-density areas corresponded to the middle cerebral artery (MCA) territory. The patient’s condition was diagnosed as newly emergent bilateral broad cerebral infarction, and the onset was presumed to be around the time of injury. On the other hand, contrast-enhanced thoracoabdominal CT obtained on the same day showed a normalized wall of the common carotid artery (Fig. 4). The patient remained comatose and eventually died 4 days after the injury. At autopsy, cervical disk rupture between C4 and C5, bilateral scapula fractures, left humerus fracture, sternal fracture, sixth dorsal vertebra fracture, bilateral multiple rib fractures, and hemothorax were found. Multiple small fissures were macroscopically observed on both the common carotid arteries (Fig. 5). Microscopically, disruption of the intima, dissection of the media, and formation of thrombus were observed (Fig. 6). The thrombus was accompanied with deposition of fibrin, and Berlin blue iron staining was negative in the thrombus. Subsequently, the thrombus may have developed at less than one week that is approximately four days, after the injury. No medial degeneration
or vasculitis at the systemic arteries, including the common carotid artery, was observed. No intraventricular thrombus, verrucous lesion at the cardiac valve, or thrombus in the major vessels, including the MCA, was observed. Tests for antibodies against human immunodeficiency virus (HIV)-1/2 and Treponema pallidum were negative.
Fig. 1. Head CT scan obtained 1 h after the accident. Arrows: sporadic, slightly lowdense areas.
Fig. 2. Contrast-enhanced CT scan obtained 1 h after the accident. Arrows: crescentshaped thickened wall of both the common carotid arteries.
3. Discussion According to the autopsy results, the cause of death was multiple chest traumas and cerebral infarction. Disturbance of consciousness (DOC) occurred shortly after the accident, and the patient remained comatose until death. Although acute alcoholic intoxication would have had an effect on the state of consciousness immediately after the accident, prolonged coma was assumed to be due to broad cerebral infarction. At autopsy, multiple small fissures were observed macroscopically, and dissection of the media and formation of thrombus were observed microscopically at the fissures. Consequently, wall thickness of both the common carotid arteries, as noticed in antemortem contrast-enhanced CT, was presumed to be due to thrombi sticking to the walls of the artery. Contrast-enhanced CT obtained 15 h after the injury showed normalized wall thickness of the artery; thus, the thrombi must have adhered to the arterial walls at the time of the first CT scan and might have been dislodged during the interval between the first and second CT scan. From these findings, the cause of cerebral infarction was suspected to be thrombi formed by CCAD. In addition, cerebral infarction due to other causes was excluded after considering the findings described below. Antemortem
F. Chiba et al. / Forensic Science International 236 (2014) e1–e4
Fig. 3. Brain CT scan obtained 15 h after the accident. A broad, low-density area within the region supplied by both the middle cerebral arteries.
electrocardiogram showed normal sinus rhythm and there was no intraventricular thrombus or verrucous lesion at the cardiac valve; thus, cardiogenic cerebral infarction was not the most likely diagnosis. Serological tests for infections that can cause multiple cerebral infarctions, such as HIV infection and syphilis, were negative. Although tuberculous meningitis may cause cephalic vasculitis and, sometimes, multiple cerebral infarctions, no stenosis or occlusion of arteries at the base of the brain was noted. Therefore, the cerebral infarction was most likely considered to be caused by artery-to-artery embolism from the thrombi formed in CCAD. Although the presence of thrombus in the MCA was not confirmed, the possibility of multiple small emboli, socalled shower embolism, which is difficult to be detected by autopsy, or of thrombolysis of unknown cause cannot be eliminated. In our case, diagnosis of CCAD during macroscopic assessment was difficult. CCAD was suspected only in antemortem contrast-enhanced CT, and the microscopic examination revealed injured arterial walls and thrombus formation. Absence of macroscopic findings such as false lumen and intramural hematoma, which are commonly observed lesions in arterial dissection, made diagnosis difficult. Thus, the diagnosis of CCAD in our case could not have been made without antemortem CT; this demonstrates the importance of antemortem clinical images in medico-legal autopsy. Table 1 summarizes the 17 cases of traumatic CCAD, including ours, reported thus far. The most frequent causes of traumatic CCAD were found to be blunt neck trauma (5 cases) and motor vehicle accidents (5 cases), followed by hanging (3 cases),
Fig. 4. Contrast-enhanced CT scan obtained 15 h after the accident. Arrows: normal wall thickness of both the common carotid arteries.
e3
Fig. 5. Multiple small fissures in both the common carotid arteries (Arrows: relatively major fissures). The fissure located on the left side of the left common carotid artery, and the largest fissure runs halfway around the right common carotid artery (the middle arrow). On antemortem CT, the fissure was located on the thickened walls of the common carotid arteries (Fig. 2).
strangulation (3 cases), and falling (1 case). The most common clinical symptoms were hemiplegia and hemiparesis. DOC occurred in only 3 cases and thus can be considered a relatively rare symptom. Only 3 cases led to a lethal complication, and 2 of the 3 fatal cases presented with DOC. Thus, DOC could be considered a sign of poor prognosis. According to the regional diagnosis from neurological symptoms and diagnostic images of the affected region, obtained using angiography, CT, or magnetic resonance imaging, the most vulnerable location was the MCA region. In our case too, both the MCA territories were infarcted. Of the 17 cases, 6 were assessed microscopically. A pathological abnormality in the arterial wall or an obliterating fibrous endarteritis was observed in only 1 of 6 cases; no arterial abnormality was observed in the other 5 cases. Thus, it could be said that traumatic CCAD could occur without any underlying condition responsible for the vulnerability. The probable mechanism of injury to the carotid artery in the case of blunt neck trauma is as follows: the carotid artery is stretched by neck hyperextension during the rotatory movement of the head, compressed against the lateral mass of the atlas and transverse processes of the spine during contralateral flexion of the neck, and directly injured by blow [12–16]. Of the 17 traumatic CCAD cases reported, bilateral CCAD occurred in 4 patients and the common causes were hanging and strangulation. This is thought to be due to direct external force acting on each side of the neck. On the other hand, among the 13 unilateral CCAD cases, the number of injuries (10) to the right side was more than thrice that to the left. Each case report does not describe the site of injury and the
Fig. 6. Microscopic disruption of the intima, dissection of the media, and formation of the thrombus.
e4
F. Chiba et al. / Forensic Science International 236 (2014) e1–e4
situation causing the injury in detail, and thus, a generalization cannot be made. However, anatomical differences may have contributed to the difference in the frequency of right- and leftsided injuries. A tentative theory suggests that one of the mechanisms of traumatic common carotid artery injury is countertraction that arises at the bifurcation of the common carotid artery via the stretched subclavian artery. This countertraction may help generate the force required to damage the common carotid artery, along with the other mechanisms mentioned above [17]. The left common carotid artery directly branches off from the aortic arch in the chest cavity, whereas the right common carotid artery branches from the brachiocephalic artery, an artery arising from the aorta, at the height of the sternoclavicular joint. In the case of blunt neck trauma, the point of bifurcation of the right common carotid artery is situated relatively closer to the head in relation to the left and is closer to the injured area. This might contribute to the greater number of right-sided injuries. In conclusion, we reported a rare case of bilateral MCA infarctions associated with traumatic CCAD. In the case of cerebral infarction with blunt neck trauma, injury of the common carotid artery could be a cause of embolism even if there is no macroscopically obvious lesion such as a false lumen or intramural hematoma. Thus, in such cases, a combined comprehensive analysis of autopsy results and antemortem clinical images is important to diagnose the exact cause of death. Conflict of interest The authors declare that they have no conflict of interest. Ethical standards This experiment complies with the current laws of the country in which it was performed.
References [1] A. Ueda, Y. Inatomi, T. Yonehara, Y. Hashimoto, T. Hirano, M. Uchino, Blunt traumatic dissection in common carotid artery with serial morphological changes detected by carotid ultrasonography in the acute phase, Rinsho Shinkeigaku 46 (2006) 631–637. [2] R. Dittrich, B. Draeger, I. Nassenstein, R. Bachmann, G. Kuhlenbaumer, D.G. Nabavi, E.B. Ringelstein, S. Evers, Dissection of the common and external carotid artery, Cerebrovasc. Dis. 21 (2006) 208–210. [3] K.F. Linnau, W.A. Cohen, Radiologic evaluation of attempted suicide by hanging: cricotracheal separation and common carotid artery dissection, AJR Am. J. Roentgenol. 178 (2002) 214. [4] Y. Okada, T. Shima, M. Nishida, K. Yamane, R. Kagawa, Traumatic dissection of the common carotid artery after blunt injury to the neck, Surg. Neurol. 51 (1999) 513–520. [5] D.G. Godfrey, V. Biousse, N.J. Newman, Delayed branch retinal artery occlusion following presumed blunt common carotid dissection, Arch. Ophthalmol. 116 (1998) 1120–1121. [6] K. Noguchi, Y. Matsuoka, K. Hohda, J. Katsuyama, S. Nishimura, A case of common carotid artery stenosis due to hanging, No Shinkei Geka 20 (1992) 1185–1188. [7] D. Oxorn, K. Clark, Crico-tracheal disruption and common carotid artery occlusion: a case of blunt trauma, Can. J. Anaesth. 37 (1990) 913–915. [8] I. Chokyu, T. Tsumoto, T. Miyamoto, H. Yamaga, T. Terada, T. Itakura, Traumatic bilateral common carotid artery dissection due to strangulation. A case report, Interv. Neuroradiol. 12 (2006) 149–154. [9] E. Furui, Y. Okamoto, S. Kida, J. Yamashita, O. Matsui, M. Yamada, Images in cardiovascular medicine. Transient occlusion of the middle cerebral artery by macroembolism during carotid stenting for traumatic dissection of the common carotid artery, Circulation 112 (2005) e33–e34. [10] A. Viaccoz, F. Perren, Focal common carotid artery intramural hematoma, J. Neuroimaging 23 (2011) 311–313. [11] F. Clarot, E. Vaz, F. Papin, B. Proust, Fatal and non-fatal bilateral delayed carotid artery dissection after manual strangulation, Forensic Sci. Int. 149 (2005) 143–150. [12] M.M. Crissey, E.F. Bernstein, Delayed presentation of carotid intimal tear following blunt craniocervical trauma, Surgery 75 (1974) 543–549. [13] J.F. Fleming, D. Petrie, Traumatic thrombosis of the internal carotid artery with delayed hemiplegia, Can. J. Surg. 11 (1968) 166–172. [14] J.B. Towne, D.D. Neis, J.W. Smith, Thrombosis of the internal carotid artery following blunt cervical trauma, Arch. Surg. 104 (1972) 565–568. [15] M.O. Perry, W.H. Snyder, E.R. Thal, Carotid artery injuries caused by blunt trauma, Ann. Surg. 192 (1980) 74–77. [16] K. Solheim, Common carotid artery aneurysm after blunt trauma, J. Trauma 19 (1979) 707–709. [17] K. Nakamura, T. Onitsuka, M. Yano, Y. Yano, T. Saitoh, K. Niina, Selective delayed management of blunt traumatic left common carotid artery injury using hypothermic circulatory arrest, Ann. Vasc. Surg. 19 (2005) 425–427.
Contents lists available at ScienceDirect
Forensic Science International journal homepage: www.elsevier.com/locate/forsciint
Case Report
Bilateral middle cerebral artery infarction associated with traumatic common carotid artery dissection: A case report and review of literature Fumiko Chiba a,*, Yohsuke Makino a,b, Ayumi Motomura a, Go Inokuchi a, Namiko Ishii a, Suguru Torimitsu a, Ayaka Sakuma a, Sayaka Nagasawa a, Hisako Saito a, Daisuke Yajima a, Mutsumi Hayakawa a, Hirotaro Iwase a a b
Department of Legal Medicine, Graduate School of Medicine, Chiba University, Inohana 1-8-1, Chuo-ku, Chiba City, Chiba Prefecture 260-8670, Japan Department of Radiology, Graduate School of Medicine, Chiba University, Inohana 1-8-1, Chuo-ku, Chiba City, Chiba Prefecture 260-8670, Japan
A R T I C L E I N F O
A B S T R A C T
Article history: Received 20 June 2013 Received in revised form 26 December 2013 Accepted 3 January 2014 Available online 10 January 2014
Traumatic common carotid artery dissection is very rare, and although it is associated with mild symptoms, it can sometimes be fatal. Therefore, careful examination of common carotid artery dissection and additional pathological examination as appropriate are important during the autopsy of traumatic death patients. A 60-year-old previously healthy drunken woman was run over. She had remained unconscious shortly after the accident, and 15 h later, emerging bilateral cerebral infarction was confirmed using brain computed tomography. Despite conservative management, she died 4 days after the injury due to multiple chest traumas and broad cerebral infarction. A medico-legal autopsy was conducted. According to the autopsy results, microscopically identified common carotid artery dissections with thrombus formation were considered the cause of infarction. In the present case, macroscopic common carotid artery lesions were relatively mild, and this made diagnosis difficult. However, the correct diagnosis was achieved by a combined analysis of the antemortem images and autopsy results. Thus, in such cases, a combined comprehensive analysis of autopsy results and antemortem clinical images is important to determine the exact cause of death. ß 2014 Elsevier Ireland Ltd. All rights reserved.
Keywords: Traumatic common carotid artery dissection Middle cerebral artery Cerebral infarction Antemortem images Forensic pathology
1. Introduction In general, common carotid artery dissection (CCAD) represents a complication of aortic dissection, and traumatic CCAD is very rare. To the best of our knowledge, only 17 articles (Table 1), including ours, on traumatic CCAD have been reported thus far in the English literature [1–11]. In addition, only one study thus far reported their findings by in-depth examination of autopsy results [11]. In this study, we describe the second autopsy case of traumatic CCAD associated with fatal cerebral infarction. 2. Case report A 60-year-old previously healthy drunken woman lying on the road was run over by a mini-vehicle. Her blood pressure was normal and spontaneous breathing was sustained. Her electrocardiogram showed a normal sinus rhythm, but she was unconscious
* Corresponding author. Tel.: +81 43 226 2078; fax: +81 43 226 2079. E-mail address: [email protected] (F. Chiba). 0379-0738/$ – see front matter ß 2014 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.forsciint.2014.01.003
when the emergency services arrived. She was brought to the hospital 30 min after the accident. She remained unconscious and was thus placed on ventilator support. Her blood level of ethanol was 286.2 mg/dL. A computed tomography scan was performed with a 128-row detector CT (Siemens Somatom Definition AS, Siemens Medical Systems, Forchheim, Germany) and the scanning protocol was as follows: tube voltage 120 kV; automatically regulated tube current: about 100–400 mA; pitch 0.8; collimation of 4.8–9.6 mm; rotation time 0.5 r/sec. DICOM image reconstruction protocol was as follows: image matrix, 525 525; slice thickness of 10 mm; field of view, 336 mm 336 mm; reconstruction kernel, B41f. A head CT taken 1 h after the accident revealed sporadic, slightly low-dense areas in both cerebral cortices (Fig. 1). Contrast-enhanced thoracoabdominal CT revealed asymmetrically thickened walls in both the common carotid arteries, and carotid artery dissection was suspected (Fig. 2). Given her general status, she was not a candidate for surgery and conservative management was begun. Head CT was performed 15 h after the injury with a 320-row detector CT (Aquilion ONE, Toshiba Medical Systems, Nasu, Japan) and the scanning protocol was as follows: tube voltage 120 kV; automatically regulated tube current: about
F. Chiba et al. / Forensic Science International 236 (2014) e1–e4
e2
Table 1 Literature review of common carotid artery dissection. Age (years), sex
Cause
Side
Clinical symptoms
Outcome
Citation
68, 37, 33, 30, 42, 58, 41, 42, 19, 50, 20, 61, 27, 43, 38, 42, 60,
Blunt neck injury Blunt neck injury Hanging injury Motor vehicle accident Motor vehicle accident Fall with neck trauma Hanging injury Blunt neck injury Motor vehicle accident Hanging injury Blunt neck injury Strangulation Blunt neck injury Motor vehicle accident Manual strangulation Manual strangulation Motor vehicle accident
Right Left Left and Right Right Right Right Right Right Right Right Left and Left Left Left and Left and Left and
Left hemiparesis, unilateral spatial neglect Neck pain Left hemiparesis Tetraplegia Left hemiparesis Left hemiparesis Dizziness Left hemiparesis, DOC (GCS score, not available) Visual loss Left upper limb weakness Left hemiparesis Tetraplegia, left hemiparesis Right hemiparesis, aphasia Difficulty finding words Right hemiparesis, DOC (GCS, 9), bilateral Babinski Headache Disturbance of consciousness (GCS, 3)
Alive Alive Alive Alive Alive Alive Alive Alive Alive Alive Dead Alive Alive Alive Dead Alive Dead
[1] [2] [3] [4] [4] [4] [4] [4] [5] [6] [7] [8] [9] [10] [11] [11] Current report
male male female female female female female male female female male female male female male female female
right
right
right right right
400 mA; pitch 0.813; collimation of 0.5 mm; rotation time 0.5 r/s. DICOM image reconstruction protocol was as follows: image matrix, 525 525; slice thickness of 10 mm; field of view, 345.1 mm 345.1 mm; reconstruction kernel, FC04. The head CT revealed broad enlarged low-density areas in both the hemispheres (Fig. 3). The distribution of low-density areas corresponded to the middle cerebral artery (MCA) territory. The patient’s condition was diagnosed as newly emergent bilateral broad cerebral infarction, and the onset was presumed to be around the time of injury. On the other hand, contrast-enhanced thoracoabdominal CT obtained on the same day showed a normalized wall of the common carotid artery (Fig. 4). The patient remained comatose and eventually died 4 days after the injury. At autopsy, cervical disk rupture between C4 and C5, bilateral scapula fractures, left humerus fracture, sternal fracture, sixth dorsal vertebra fracture, bilateral multiple rib fractures, and hemothorax were found. Multiple small fissures were macroscopically observed on both the common carotid arteries (Fig. 5). Microscopically, disruption of the intima, dissection of the media, and formation of thrombus were observed (Fig. 6). The thrombus was accompanied with deposition of fibrin, and Berlin blue iron staining was negative in the thrombus. Subsequently, the thrombus may have developed at less than one week that is approximately four days, after the injury. No medial degeneration
or vasculitis at the systemic arteries, including the common carotid artery, was observed. No intraventricular thrombus, verrucous lesion at the cardiac valve, or thrombus in the major vessels, including the MCA, was observed. Tests for antibodies against human immunodeficiency virus (HIV)-1/2 and Treponema pallidum were negative.
Fig. 1. Head CT scan obtained 1 h after the accident. Arrows: sporadic, slightly lowdense areas.
Fig. 2. Contrast-enhanced CT scan obtained 1 h after the accident. Arrows: crescentshaped thickened wall of both the common carotid arteries.
3. Discussion According to the autopsy results, the cause of death was multiple chest traumas and cerebral infarction. Disturbance of consciousness (DOC) occurred shortly after the accident, and the patient remained comatose until death. Although acute alcoholic intoxication would have had an effect on the state of consciousness immediately after the accident, prolonged coma was assumed to be due to broad cerebral infarction. At autopsy, multiple small fissures were observed macroscopically, and dissection of the media and formation of thrombus were observed microscopically at the fissures. Consequently, wall thickness of both the common carotid arteries, as noticed in antemortem contrast-enhanced CT, was presumed to be due to thrombi sticking to the walls of the artery. Contrast-enhanced CT obtained 15 h after the injury showed normalized wall thickness of the artery; thus, the thrombi must have adhered to the arterial walls at the time of the first CT scan and might have been dislodged during the interval between the first and second CT scan. From these findings, the cause of cerebral infarction was suspected to be thrombi formed by CCAD. In addition, cerebral infarction due to other causes was excluded after considering the findings described below. Antemortem
F. Chiba et al. / Forensic Science International 236 (2014) e1–e4
Fig. 3. Brain CT scan obtained 15 h after the accident. A broad, low-density area within the region supplied by both the middle cerebral arteries.
electrocardiogram showed normal sinus rhythm and there was no intraventricular thrombus or verrucous lesion at the cardiac valve; thus, cardiogenic cerebral infarction was not the most likely diagnosis. Serological tests for infections that can cause multiple cerebral infarctions, such as HIV infection and syphilis, were negative. Although tuberculous meningitis may cause cephalic vasculitis and, sometimes, multiple cerebral infarctions, no stenosis or occlusion of arteries at the base of the brain was noted. Therefore, the cerebral infarction was most likely considered to be caused by artery-to-artery embolism from the thrombi formed in CCAD. Although the presence of thrombus in the MCA was not confirmed, the possibility of multiple small emboli, socalled shower embolism, which is difficult to be detected by autopsy, or of thrombolysis of unknown cause cannot be eliminated. In our case, diagnosis of CCAD during macroscopic assessment was difficult. CCAD was suspected only in antemortem contrast-enhanced CT, and the microscopic examination revealed injured arterial walls and thrombus formation. Absence of macroscopic findings such as false lumen and intramural hematoma, which are commonly observed lesions in arterial dissection, made diagnosis difficult. Thus, the diagnosis of CCAD in our case could not have been made without antemortem CT; this demonstrates the importance of antemortem clinical images in medico-legal autopsy. Table 1 summarizes the 17 cases of traumatic CCAD, including ours, reported thus far. The most frequent causes of traumatic CCAD were found to be blunt neck trauma (5 cases) and motor vehicle accidents (5 cases), followed by hanging (3 cases),
Fig. 4. Contrast-enhanced CT scan obtained 15 h after the accident. Arrows: normal wall thickness of both the common carotid arteries.
e3
Fig. 5. Multiple small fissures in both the common carotid arteries (Arrows: relatively major fissures). The fissure located on the left side of the left common carotid artery, and the largest fissure runs halfway around the right common carotid artery (the middle arrow). On antemortem CT, the fissure was located on the thickened walls of the common carotid arteries (Fig. 2).
strangulation (3 cases), and falling (1 case). The most common clinical symptoms were hemiplegia and hemiparesis. DOC occurred in only 3 cases and thus can be considered a relatively rare symptom. Only 3 cases led to a lethal complication, and 2 of the 3 fatal cases presented with DOC. Thus, DOC could be considered a sign of poor prognosis. According to the regional diagnosis from neurological symptoms and diagnostic images of the affected region, obtained using angiography, CT, or magnetic resonance imaging, the most vulnerable location was the MCA region. In our case too, both the MCA territories were infarcted. Of the 17 cases, 6 were assessed microscopically. A pathological abnormality in the arterial wall or an obliterating fibrous endarteritis was observed in only 1 of 6 cases; no arterial abnormality was observed in the other 5 cases. Thus, it could be said that traumatic CCAD could occur without any underlying condition responsible for the vulnerability. The probable mechanism of injury to the carotid artery in the case of blunt neck trauma is as follows: the carotid artery is stretched by neck hyperextension during the rotatory movement of the head, compressed against the lateral mass of the atlas and transverse processes of the spine during contralateral flexion of the neck, and directly injured by blow [12–16]. Of the 17 traumatic CCAD cases reported, bilateral CCAD occurred in 4 patients and the common causes were hanging and strangulation. This is thought to be due to direct external force acting on each side of the neck. On the other hand, among the 13 unilateral CCAD cases, the number of injuries (10) to the right side was more than thrice that to the left. Each case report does not describe the site of injury and the
Fig. 6. Microscopic disruption of the intima, dissection of the media, and formation of the thrombus.
e4
F. Chiba et al. / Forensic Science International 236 (2014) e1–e4
situation causing the injury in detail, and thus, a generalization cannot be made. However, anatomical differences may have contributed to the difference in the frequency of right- and leftsided injuries. A tentative theory suggests that one of the mechanisms of traumatic common carotid artery injury is countertraction that arises at the bifurcation of the common carotid artery via the stretched subclavian artery. This countertraction may help generate the force required to damage the common carotid artery, along with the other mechanisms mentioned above [17]. The left common carotid artery directly branches off from the aortic arch in the chest cavity, whereas the right common carotid artery branches from the brachiocephalic artery, an artery arising from the aorta, at the height of the sternoclavicular joint. In the case of blunt neck trauma, the point of bifurcation of the right common carotid artery is situated relatively closer to the head in relation to the left and is closer to the injured area. This might contribute to the greater number of right-sided injuries. In conclusion, we reported a rare case of bilateral MCA infarctions associated with traumatic CCAD. In the case of cerebral infarction with blunt neck trauma, injury of the common carotid artery could be a cause of embolism even if there is no macroscopically obvious lesion such as a false lumen or intramural hematoma. Thus, in such cases, a combined comprehensive analysis of autopsy results and antemortem clinical images is important to diagnose the exact cause of death. Conflict of interest The authors declare that they have no conflict of interest. Ethical standards This experiment complies with the current laws of the country in which it was performed.
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