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A case of aneurysmal rupture at the vertebral artery 14 days after whiplash injury: was it traumatic or non-traumatic?
Legal Medicine 5 (2003) 69–71 www.elsevier.com/locate/legalmed
Letter to the Editor A case of aneurysmal rupture at the vertebral artery 14 days after whiplash injury: was it traumatic or non-traumatic? To the Editor: This report presents a case of subarachnoid hemorrhage (SAH) caused by a tear in an intracranial vertebral artery, and discusses whether the tear in the vertebral artery aneurysm interacted with acceleration trauma to the neck sustained 14 days earlier. A 48-year-old male experienced pain in his neck when the taxi in which he was riding came to an abrupt halt. There were no obvious injuries on X-ray examination, thus he was diagnosed as having a whiplash injury. He consulted the hospital several times, since pain and stiffness around the neck persisted. Fourteen days after he was injured, his mother found him dead in bed when she tried to wake him up at 7 o’clock am. He had no remarkable medical history before the incident, and it was not known whether he was hypertensive. We were requested to clarify whether the incident was related to death. Autopsy was performed about 24 h postmortem. The body was 162 cm high and weighed 69 kg. Rigor mortis was observed in all joints. Light reddish-purple lividity was present on the back. The face was pale, and several conjunctival petechiae were observed bilaterally. Internally, there was a small amount of yellow fluid in the thoracic and abdominal cavities. The heart (370 g) contained fluid and clotted blood. Mild atherosclerosis was found in the aorta. The lungs (left: 650 g, right: 630 g) did not demonstrate any remarkable change on the external surface, although a large amount of frothy fluid exuded from the cut surfaces. Ethanol was detected at a concentration of 0.22 mg/ml in the urine (400 ml) and 0.13 mg/ml in the blood. The brain weighed 1640 g with mild edema. SAH was observed at the front and temporal lobes of the
cerebrum, the inferior surfaces of the brain stem and cerebellum. A 3 cm long fusiform dilatation with a 0.2 cm longitudinal tear was observed in the right vertebral artery, 1 cm distal to the origin of the basilar artery (Fig. 1). On microscopic observation, the wall of the right vertebral artery showed a different thickness at the fusiform area. About one-half of the wall containing the tear was thin and lacked internal elastic fibers, while the opposite wall was thick with flabby internal elastic fibers (Fig. 2). In the thickened wall, three cleft-like blood-filled cavities were present. The internal elastic fibers near the blood cavity were extended and disrupted. Only a few hemosiderin granules were detected near the cavities. The bloodfilled cavities and disruption of elastic fiber suggested that these were caused by dissection, although the
Fig. 1. Subarachnoid hemorrhage (SAH) at the inferior surface of the brain. A tear in the fusiform-like aneurysm in the right vertebral artery was observed.
1344-6223/02/$ - see front matter q 2002 Elsevier Science Ireland Ltd. All rights reserved. doi:10.1016/S1344-6223(02)00073-1
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Y. Nishitani et al. / Legal Medicine 5 (2003) 69–71
Fig. 2. Photomicrograph of the vertebral artery at the rupture (axial slice). The wall demonstrated unequal thickness, and ruptured at the thinned section. Internal elastic fiber disruption and blood cavities in media tunica were apparent in the thick wall section. (Elastica van Gieson, £ 20).
entry into the vessel wall could not be identified. There was no infiltration of leucocytes around the tear. The boundary between the thin and thick segments in the wall was clear, and the ends of the disrupted elastic fiber were clearly observed. Only mild atheroma was found in the left vertebral artery. The wall containing the tear was thin and lacked internal elastic fibers in the present case. The inner elastic fibers do not seem to have been disrupted or fragmented by old hemorrhage or dissection because there were no hemosiderin granules detected in the thinned section. It was unclear why the inner elastic fiber was absent. The thin wall segment may be congenitally lacking in internal elastic fibers [1]. In contrast, the thickened parts containing blood-filled cavities were formed by a new dissection since the hemorrhages were fresh, with only a few hemosiderin granules. Aneurysm formation and its rupture may have been the result of disequilibration between arterial wall strength and hemodynamic stress [1,2]. Probably the production of blood cavities induced by hemodynamic stress caused a tear in the thin part of the arterial wall. Aneurysmal rupture at the vertebral artery occurred due to either traumatic or non-traumatic factors. However, it is sometimes difficult to distinguish which of the two was involved [3 – 9]. When an aneurysm ruptures, it causes SAH. The vertebral
artery injury is sometimes caused by a blunt force to the head or neck, and the survival interval is usually short after injury. Opeskin et al. reviewed 30 cases of vertebral artery injury. Most cases could not survive more than 1 day after injury, although two cases survival for several weeks after injury [3]. Therefore, the aneruysmal rupture causing SAH was considered non-traumatic in this case. We conclude that the dissection in the present case was spontaneous, and that there was no relationship between the whiplash injury and the aneurysmal rupture. Although the man was estimated to have died early in the morning by spontaneous SAH, it is reported that the occurrence of SAH during rest or sleep is not rare (11.8%) [10].
References [1] Mizutani T, Miki Y, Kojima H, Suzuki H. Proposed classification of non-atherosclerotic cerebral fusiform and dissecting aneurysms. Neurosurgery 1999;45:253–9. [2] Farag AM, Franks A, Gee DJ. Simple laboratory experiments to replicate some of the stresses on vertebro-basilar arterial walls. An investigation of possible mechanisms of traumatic subarachnoid haemorrhage. Forensic Sci Int 1988;38:275–84. [3] Opeskin K, Burke MP. Vertebral artery trauma. Am J Forensic Med Pathol 1998;19:206 –17. [4] Gray JT, Puetz SM, Jackson SL, Green MA. Traumatic subarachnoid haemorrhage: a 10-year case study and review. Forensic Sci Int 1999;1.5:13 –23.
Y. Nishitani et al. / Legal Medicine 5 (2003) 69–71 [5] Schievink WI. Spontaneous dissection of the carotid and vertebral arteries. N Engl J Med 2001;344:898 –906. [6] Pollanen MS, Dech JHN, Blenkinsop B. Injury of the tunica media in fatal rupture of the vertebral artery. Am J Forensic Med Pathol 1996;17:197–201. [7] Klages U. Spontane oder traumatische to¨dliche Subarachnoidalblutung. Z Rechtsmed 1970;67:67–86. [8] Gonsoulin M, Barnard JJ, Prahlow JA. Death resulting from ruptured cerebral artery aneurysm: 219 cases. Am J Forensic Med Pathol 2002;23:5–14. [9] Bauer M, Lang C, Patzelt D. Sudden death due to pituitary apoplexy. Legal Med 2001;3:183 –6. [10] Schievink WI, Karemaker JM, Hageman LM, van der Werf DJ. Circumstances surrounding aneurysmal subarachnoid hemorrhage. Surg Neurol 1989;32:266–72.
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Yoko Nishitanip,1, Tamaki Hayase, Yoshiko Yamamoto, Keiichi Yamamoto, Keiji Tamaki Department of Legal Medicine, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan1 * Corresponding author. Tel.: þ 81-75-753-4474; fax: þ81-75761-9591. E-mail address: [email protected] (Y. Nishitani).
Letter to the Editor A case of aneurysmal rupture at the vertebral artery 14 days after whiplash injury: was it traumatic or non-traumatic? To the Editor: This report presents a case of subarachnoid hemorrhage (SAH) caused by a tear in an intracranial vertebral artery, and discusses whether the tear in the vertebral artery aneurysm interacted with acceleration trauma to the neck sustained 14 days earlier. A 48-year-old male experienced pain in his neck when the taxi in which he was riding came to an abrupt halt. There were no obvious injuries on X-ray examination, thus he was diagnosed as having a whiplash injury. He consulted the hospital several times, since pain and stiffness around the neck persisted. Fourteen days after he was injured, his mother found him dead in bed when she tried to wake him up at 7 o’clock am. He had no remarkable medical history before the incident, and it was not known whether he was hypertensive. We were requested to clarify whether the incident was related to death. Autopsy was performed about 24 h postmortem. The body was 162 cm high and weighed 69 kg. Rigor mortis was observed in all joints. Light reddish-purple lividity was present on the back. The face was pale, and several conjunctival petechiae were observed bilaterally. Internally, there was a small amount of yellow fluid in the thoracic and abdominal cavities. The heart (370 g) contained fluid and clotted blood. Mild atherosclerosis was found in the aorta. The lungs (left: 650 g, right: 630 g) did not demonstrate any remarkable change on the external surface, although a large amount of frothy fluid exuded from the cut surfaces. Ethanol was detected at a concentration of 0.22 mg/ml in the urine (400 ml) and 0.13 mg/ml in the blood. The brain weighed 1640 g with mild edema. SAH was observed at the front and temporal lobes of the
cerebrum, the inferior surfaces of the brain stem and cerebellum. A 3 cm long fusiform dilatation with a 0.2 cm longitudinal tear was observed in the right vertebral artery, 1 cm distal to the origin of the basilar artery (Fig. 1). On microscopic observation, the wall of the right vertebral artery showed a different thickness at the fusiform area. About one-half of the wall containing the tear was thin and lacked internal elastic fibers, while the opposite wall was thick with flabby internal elastic fibers (Fig. 2). In the thickened wall, three cleft-like blood-filled cavities were present. The internal elastic fibers near the blood cavity were extended and disrupted. Only a few hemosiderin granules were detected near the cavities. The bloodfilled cavities and disruption of elastic fiber suggested that these were caused by dissection, although the
Fig. 1. Subarachnoid hemorrhage (SAH) at the inferior surface of the brain. A tear in the fusiform-like aneurysm in the right vertebral artery was observed.
1344-6223/02/$ - see front matter q 2002 Elsevier Science Ireland Ltd. All rights reserved. doi:10.1016/S1344-6223(02)00073-1
70
Y. Nishitani et al. / Legal Medicine 5 (2003) 69–71
Fig. 2. Photomicrograph of the vertebral artery at the rupture (axial slice). The wall demonstrated unequal thickness, and ruptured at the thinned section. Internal elastic fiber disruption and blood cavities in media tunica were apparent in the thick wall section. (Elastica van Gieson, £ 20).
entry into the vessel wall could not be identified. There was no infiltration of leucocytes around the tear. The boundary between the thin and thick segments in the wall was clear, and the ends of the disrupted elastic fiber were clearly observed. Only mild atheroma was found in the left vertebral artery. The wall containing the tear was thin and lacked internal elastic fibers in the present case. The inner elastic fibers do not seem to have been disrupted or fragmented by old hemorrhage or dissection because there were no hemosiderin granules detected in the thinned section. It was unclear why the inner elastic fiber was absent. The thin wall segment may be congenitally lacking in internal elastic fibers [1]. In contrast, the thickened parts containing blood-filled cavities were formed by a new dissection since the hemorrhages were fresh, with only a few hemosiderin granules. Aneurysm formation and its rupture may have been the result of disequilibration between arterial wall strength and hemodynamic stress [1,2]. Probably the production of blood cavities induced by hemodynamic stress caused a tear in the thin part of the arterial wall. Aneurysmal rupture at the vertebral artery occurred due to either traumatic or non-traumatic factors. However, it is sometimes difficult to distinguish which of the two was involved [3 – 9]. When an aneurysm ruptures, it causes SAH. The vertebral
artery injury is sometimes caused by a blunt force to the head or neck, and the survival interval is usually short after injury. Opeskin et al. reviewed 30 cases of vertebral artery injury. Most cases could not survive more than 1 day after injury, although two cases survival for several weeks after injury [3]. Therefore, the aneruysmal rupture causing SAH was considered non-traumatic in this case. We conclude that the dissection in the present case was spontaneous, and that there was no relationship between the whiplash injury and the aneurysmal rupture. Although the man was estimated to have died early in the morning by spontaneous SAH, it is reported that the occurrence of SAH during rest or sleep is not rare (11.8%) [10].
References [1] Mizutani T, Miki Y, Kojima H, Suzuki H. Proposed classification of non-atherosclerotic cerebral fusiform and dissecting aneurysms. Neurosurgery 1999;45:253–9. [2] Farag AM, Franks A, Gee DJ. Simple laboratory experiments to replicate some of the stresses on vertebro-basilar arterial walls. An investigation of possible mechanisms of traumatic subarachnoid haemorrhage. Forensic Sci Int 1988;38:275–84. [3] Opeskin K, Burke MP. Vertebral artery trauma. Am J Forensic Med Pathol 1998;19:206 –17. [4] Gray JT, Puetz SM, Jackson SL, Green MA. Traumatic subarachnoid haemorrhage: a 10-year case study and review. Forensic Sci Int 1999;1.5:13 –23.
Y. Nishitani et al. / Legal Medicine 5 (2003) 69–71 [5] Schievink WI. Spontaneous dissection of the carotid and vertebral arteries. N Engl J Med 2001;344:898 –906. [6] Pollanen MS, Dech JHN, Blenkinsop B. Injury of the tunica media in fatal rupture of the vertebral artery. Am J Forensic Med Pathol 1996;17:197–201. [7] Klages U. Spontane oder traumatische to¨dliche Subarachnoidalblutung. Z Rechtsmed 1970;67:67–86. [8] Gonsoulin M, Barnard JJ, Prahlow JA. Death resulting from ruptured cerebral artery aneurysm: 219 cases. Am J Forensic Med Pathol 2002;23:5–14. [9] Bauer M, Lang C, Patzelt D. Sudden death due to pituitary apoplexy. Legal Med 2001;3:183 –6. [10] Schievink WI, Karemaker JM, Hageman LM, van der Werf DJ. Circumstances surrounding aneurysmal subarachnoid hemorrhage. Surg Neurol 1989;32:266–72.
71
Yoko Nishitanip,1, Tamaki Hayase, Yoshiko Yamamoto, Keiichi Yamamoto, Keiji Tamaki Department of Legal Medicine, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan1 * Corresponding author. Tel.: þ 81-75-753-4474; fax: þ81-75761-9591. E-mail address: [email protected] (Y. Nishitani).