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Fatal traumatic aneurysm of the posterior inferior cerebellar artery with delayed rupture
Forensic Science International 247 (2015) e1–e5
Contents lists available at ScienceDirect
Forensic Science International journal homepage: www.elsevier.com/locate/forsciint
Case Report
Fatal traumatic aneurysm of the posterior inferior cerebellar artery with delayed rupture Bibianna Purgina a,b, Christopher Mark Milroy a,b,* a Eastern Ontario Forensic Pathology Unit of the Ontario Forensic Pathology Service, Department of Anatomical Pathology, Eastern Ontario Regional Laboratory Service, The Ottawa Hospital, Ottawa, Canada b Department of Pathology and Laboratory Medicine, University of Ottawa, Ottawa, Canada
A R T I C L E I N F O
A B S T R A C T
Article history: Received 27 October 2014 Accepted 2 November 2014 Available online 3 December 2014
Traumatic aneurysms of intracranial arteries are rare, forming less than 1% of all intracranial arteries. They may be associated with penetrating and non-penetrating trauma. Most cases are associated with fracturing of the skull. Rupture of traumatic aneurysms occur in up to 50% of cases and are typically delayed from days to weeks following the initiating trauma. We report a case of a 22-year-old man who was punched to the head. He was rendered unconscious but recovered and had a GCS of 14 on admission. CT scans showed subarachnoid hemorrhage. An initial angiogram was negative but on day 7 following the incident he was noted to have a 1 mm aneurysm of the posterior inferior cerebellar artery on CT angiogram. On day 9 he collapsed and was found to have new subarachnoid hemorrhage and to have a 4.0 mm 3.7 mm. He did not recover and was declared brain dead on day 12. At autopsy, there was a 4.0 mm aneurysm of the left PICA just after the origin of the artery. Histological examination confirmed the presence of a traumatic false aneurysm in the left PICA. This case study shows sequential radiological imaging with pathologiocal correlation. ß 2014 Elsevier Ireland Ltd. All rights reserved.
Keywords: Aneurysm Traumatic Intracranial False Rupture PICA
1. Introduction Blunt trauma to the head and neck can produce a variety of injuries. Blunt trauma to the neck can cause severe injury to the vertebral and carotid arteries. Blunt trauma to the head can produce more types of injuries based on a variety of mechanisms. Acceleration injuries can produce focal or diffuse injury to the axons and blunt trauma can also cause injury to the intracranial distal portions of the carotid arteries (anterior cerebral arteries) and posterior vessels. Intracranial traumatic aneurysms are extremely rare and are associated with blunt or penetrating injury and most reported cases have been associated with a skull fracture [1–6]. They make up less than 1% of all intracranial aneurysms and are more common in children and males due to increased incidence of trauma [2,3,7,8]. Mao and colleagues found 15 cases following blunt trauma out of 2335 intracranial aneurysms (0.64%) with motor vehicle collisions accounting for 10 cases and falls for the other * Corresponding author at: Division of Anatomical Pathology, The Ottawa Hospital, 501 Smyth Road, Ottawa K1H 8L6, Canada. Tel.: +1 613 737 8899 ex 79812. E-mail address: [email protected] (C.M. Milroy). http://dx.doi.org/10.1016/j.forsciint.2014.11.003 0379-0738/ß 2014 Elsevier Ireland Ltd. All rights reserved.
5 cases [8]. They also had 1 case with penetrating trauma and 4 iatrogenic cases. Aneurysms of the superior and posterior inferior cerebellar arteries have been reported with and without associated skull fracturing [9,10]. The clinical presentation is variable, with subarachnoid hemorrhage (SAH), acute loss of consciousness, seizures, and neurological deficits appearing immediately or months to years later [1–4]. Histologically, traumatic aneurysms have been classified by Burton according to the types of vascular trauma and aneurysms produced, which are true aneurysms, false aneurysms, and mixed or dissecting aneurysms [1]. True aneurysms involve three intact arterial wall layers and demonstrate a partial disruption of the arterial wall leading to weakening and aneurysm formation secondary to flow dynamics. False aneurysms are considered to be the most common histological type associated with head trauma and result from disruption of all three layers of the vessel wall with formation of a contained hematoma surrounded by adventitia and periadventitial tissues and communicating with the vessel lumen. False aneurysms grow faster than true aneurysms, and their risk of re-bleeding is very high. Mixed aneurysm describes rupture of a true aneurysm leading to the formation of a false aneurysm.
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B. Purgina, C.M. Milroy / Forensic Science International 247 (2015) e1–e5
Fig. 1. A conventional catheter angiogram showing no evidence of an aneurysm or fistula.
We report a case of traumatic aneurysm of the left posterior inferior cerebellar artery (PICA) in young man following a punch to the head, without any penetrating injury or skull fracture.
2. Case report A 22-year-old man attempted to break up the fight between two other men and was struck at least once to the head. He collapsed immediately and was unconscious. Initial assessment by paramedics at the scene determined that he had a Glasgow Coma Scale (GCS) score of 3/4 and he required ventilatory support with a bag. His pupils were dilated and deviated to the left. Overall he appeared post-ictal to the paramedics. At the emergency department, he was noted to have a GCS of 14. Abrasions were noted to the left brow, right forehead and there was vomitus in the left ear. Subsequently his GCS fluctuated from 11 to 14 and he was ventilated and admitted to the intensive care unit. Initial CT scan showed diffuse moderate SAH and intraventricular hemorrhage (IVH) as well as mild hydrocephalus. A conventional catheter angiogram showed no evidence of obvious aneurysm or fistula (Fig. 1). No evidence of vasospasm was seen. An admission blood ethanol was 39 mmol/L (177 mg/100 ml). On Day 2, the patient was extubated. Subsequently he had a GCS score of 15, although he complained of headaches and some memory loss. A CT scan done on Day 2 showed slight progression of the hydrocephalus. On Day 7, CT scan of the brain without contrast and CT angiogram of the circle of Willis was performed. There was minimal residual blood in the right occipital horn. Previously documented SAH had completely resolved. The minimal ventricular prominence was unchanged. There was no evidence of infarction seen and no evidence of extra axial collection was seen. CT angiogram performed demonstrated a tiny 1.0 mm aneurysm at the origin of the left PICA (Fig. 2). There was a normal appearance to the rest of the intracranial arteries. There was no other aneurysm or arterio-venous malformation noted. By Day 9 he was fully mobilizing and had left the ward to go to smoke a cigarette, a friend described him as going limp and being unresponsive. Following this collapse, he had a GCS of 3. CT scan was performed which showed that there was new IVH and SAH in the left cerebellopontine angle region and at the level of the foramen magnum. This was in keeping with a ruptured aneurysm of the left PICA. A 4.0 mm 3.7 mm aneurysm of the left PICA was demonstrated (Fig. 3).
A further CT scan conducted on Day 10 showed little change and extensive SAH and IVH remaining. He developed fixed dilated pupils and his condition did not improve. Brain stem death was confirmed on Day 12. The findings at autopsy included were that the brain was markedly swollen, weighing 1700 g, and tonsillar grooving was evident. No contusional damage of the brain parenchyma was identified and there were no focal lesions seen on sectioning of the brain. SAH was most notable around the origin of the left PICA. Examination of the circle of Willis demonstrated a 4.0 mm aneurysm of the left PICA just after the origin of the artery (Fig. 4). The remaining vessels of the circle of Willis appeared normal. Histological examination (Figs. 5 and 6) confirmed the presence of a traumatic false aneurysm in the left PICA. The rupture site was demonstrtaed (Fig. 7). Aneurysmal dilation was composed of adventitial tissue partially surrounding a hematoma (Fig. 8). The distal end of the aneurysm, that is the side opposite the aneurysm mouth, had ruptured. No hemosiderin staining was present and
Fig. 2. CT angiogram performed on day 7 demonstrated a tiny 1.0 mm aneurysm at the origin of the left PICA.
B. Purgina, C.M. Milroy / Forensic Science International 247 (2015) e1–e5
Fig. 3. CT angiogram performed on day 9. There was a 4.0 3.7 mm aneurysm of the left PICA.
Fig. 4. 4.0 mm aneurysm of the left PICA just after the origin of the artery.
Fig. 5. Traumatic false aneurysm in the left PICA (hemotoxylin and eosin).
Fig. 6. Traumatic false aneurysm in the left PICA (Masson trichrome).
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B. Purgina, C.M. Milroy / Forensic Science International 247 (2015) e1–e5
e4
Fig. 7. Traumatic false aneurysm rupture site (Movat stain).
Fig. 9. Corpus callosum necrosis, with hemosiderin and red blood cells identified (a and b). Fig. 8. Aneurysmal dilation with adventitial tissue partially surrounding a hematoma.
there was no evidence of a long-standing aneurysm. The arteries of the circle of Willis showed no underlying abnormality. Neurohistology confirmed the presence of established hypoxic changes throughout the brain with prominent cerebral edema. In the corpus callosum there were areas of necrosis, with hemosiderin and red blood cells identified (Fig. 9a and b). There are obvious axonal retraction balls in these areas. Stains for beta-amyloid precursor protein (b-APP) were positive confirming axonal damage in the corpus callosum. 3. Discussion Traumatic aneurysms are very rare. Most are located near the midline or base of skull, in the region of the circle of Willis, mainly affecting the middle cerebral artery, anterior cerebral artery, or internal carotid artery [1–6]. Less than 10% involve the posterior circulation and are associated with SAH and brain stem ischemia [8]. Approximately 50% of reported cases of traumatic aneurysms undergo delayed rupture, with an average interval 14–21 days [1– 6]. The mortality rate varies between 32–54% in untreated cases and 18–24% after surgical management [3,5]. The majority of traumatic aneurysms have been reported as result of direct vascular injury secondary to skull fracture or penetrating injury [5,11]. Rarely they form as a result of shearing forces causing torsion and overstretching of the vessels of the
arteries at the time of trauma [5,11], though the frequency of the cause of traumatic aneurysms may depend on local factors. A report of 13 cases from Israel involved 7 explosions, 2 gunshot wounds, 2 motor vehicle collisions, one stabbing and on fall from a height [12]. Bell and colleagues reported on 64 military cases [13]. In our patient, blunt craniocervical trauma creating acceleration and deceleration of the cerebellum within the skull injuring the PICA at its origin, explains the formation of a traumatic aneurysm of the left PICA and traumatic axonal injury in the corpus callosum. Traumatic aneurysms should be suspected in the setting of acute neurological deterioration following any type of closed head injury and patients should undergo immediate CT scanning. If the scan demonstrates SAH in a pattern suggestive of aneurysmal SAH (IVH with SAH or posterior fossa SAH), an angiogram usually follows to look for vascular injury [5,11]. CT features suggestive of PICA aneurysm rupture include IVH with hydrocephalus, seen in 90% of cases [11]. It is rare to see SAH at the level of cerebral convexities in ruptured PICA aneurysms [11]. In this case, our patient demonstrated at presentation to hospital fluctuating GCS and initial imaging demonstrated the presence of IVH with hydrocephalus and SAH concentrated around the basal circulation of the brain, typical pattern of rupture PICA aneurysm [9]. Initial catheter angiogram did not reveal the presence of an aneurysm. A week later imaging confirmed complete resolution of the SAH and a CT angiogram demonstrated a newly formed 1.0 mm aneurysm at the origin of the left PICA. Two days later, the aneurysm had enlarged and ruptured causing massive neurologic injury leading to death. At presentation, our patient had a blood
B. Purgina, C.M. Milroy / Forensic Science International 247 (2015) e1–e5
ethanol concentration of 39 mmol/L (177 mg/100 mL). A degree of motor and cognitive in-coordination is expected, however it did not directly contributed to his death. Even though more than 100 cases of traumatic aneurysms are reported in the literature, most are associated with penetrating head injuries and skull fractures. Traumatic aneurysms involving the vertebral artery or the PICA are extremely rare, with only 10 other cases in the literature. Eight of these cases are associated with skull fracture. To the best of our knowledge, this is the only case with imaging demonstrating the evolution of the traumatic aneurysm and pathological correlation. When dealing with aneurysmal bleeding following trauma, one wonders whether a pre-existing berry aneurysm has ruptured due to mechanical damage or arterial hypertension [5]. Sequential imaging in this case proves without a doubt that this is a traumainduced aneurysm. Strictly speaking, the diagnosis of traumatic aneurysms would require proof of their formation after head trauma by comparing pre- and post-traumatic angiographic studies [14]. Other features that are useful to distinguish a traumatic aneurysm from a natural ‘‘berry’’ aneurysm include young male, history of trauma and angiographic features including peripheral location, site away from a branching point, irregular outline of the sac, absence of neck, delayed filling and emptying and location adjacent to the falx edge [15,16]. Traumatic aneurysms are often fragile, prone to rupture and present a challenge for either surgical or endovascular therapy. The goal of managing patients with traumatic aneurysms is early diagnosis and intervention to prevent delayed-onset re-bleeding or other thromboembolic complications.
e5
References [1] C. Burton, F. Velasco, J. Dorman, Traumatic aneurysm of a peripheral cerebral artery: review and case report, J. Neurosurg. 28 (1968) 468–474. [2] B.G. Benoit, G. Wortzman, Traumatic cerebral aneurysms. Clinical features and natural history, J. Neurol. Neurosurg. Psychiatry 36 (1973) 127–138. [3] S. Asari, S. Nakamura, O. Yamada, H. Beck, H. Sugatani, H. Higashi, Traumatic aneurysm of peripheral cerebral arteries, J. Neurosurg. 46 (1977) 795–803. [4] B. Holmes, R.E. Harbaugh, Traumatic intracranial aneurysms: a contemporary review, J. Trauma 35 (1993) 855–860. [5] T. Nishioka, Y. Maeda, Y. Tomogane, A. Nakano, N. Arita, Unexpected delayed rupture of vertebral-posterior inferior cerebellar artery aneurysms following closed head Injury, Acta Neurochir. 144 (2002) 839–845. [6] M.R. Frusco, M.R. Harrigan, Cerebrovascular dissections: a review. Part II: blunt cerebrovascular injury, Neurosurgery 68 (2011) 517–530. [7] T.-C. Yang, Y.-L. Lo, Y.-C. Huang, S.-T. Yang, Traumatic anterior cerebral artery aneurysm following blunt craniofacial trauma, Eur. Neurol. 58 (2007) 239–245. [8] Z. Mao, N. Wang, M. Hussain, et al., Traumatic intracranial aneurysms due to blunt brain injury – a single centre experience, Acta Neurochir. 154 (2012) 2187–2193. [9] H. Yamakawa, Y. Kaku, S. Yoshimura, A. Ohkuma, N. Sakai, Two cases of dissecting aneurysm of the distal posterior inferior cerebellar artery: possible involvement of segmental mediolytic arteriopathy in the pathogenesis, Clin. Neurol. Neurosurg. 107 (2005) 117–122. [10] N. Morard m de Tribolet, Traumatic aneurysm of the posterior inferior cerebellar artery: case report, Neurosurgery 29 (1991) 438–439. [11] W.S. Paiva, A.F. Andrade, H.S. Neto, et al., Traumatic pseudoaneurysm of the superior cerebellar artery, J. Trauma 72 (2011) E115. [12] J.E. Cohen, J.M. Gomori, R. Segal, et al., Results of endovascular treatment of traumatic intracranial aneurysms, Neurosurgery 63 (2008) 476–484. [13] R.S. Bell, A.H. Vo, R. Roberts, et al. Neurosurgery 66 (2010) 66–79. [14] D. Kallmes, G. Lanzino, J.E. Dix, J.E. Dion, H. Do, R.J. Woodcock, N.F. Kassell, Patterns of hemorrhage with ruptured posterior inferior cerebellar artery aneurysms: CT findings in 44 cases, Am. J. Rad. 169 (1997) 1169–1171. [15] F. Quintana, C. Diez, A. Gutierrez, M.L. Diez, O. Austin, A. Vazquez, Traumatic aneurysm of the basilar artery, Am. J. Neuroradiol. 17 (1994) 283–285. [16] K. Opeskin, Traumatic pericallosal artery aneurysm, Am. J. Forensic Med. Pathol. 16 (1995) 11–16.
Contents lists available at ScienceDirect
Forensic Science International journal homepage: www.elsevier.com/locate/forsciint
Case Report
Fatal traumatic aneurysm of the posterior inferior cerebellar artery with delayed rupture Bibianna Purgina a,b, Christopher Mark Milroy a,b,* a Eastern Ontario Forensic Pathology Unit of the Ontario Forensic Pathology Service, Department of Anatomical Pathology, Eastern Ontario Regional Laboratory Service, The Ottawa Hospital, Ottawa, Canada b Department of Pathology and Laboratory Medicine, University of Ottawa, Ottawa, Canada
A R T I C L E I N F O
A B S T R A C T
Article history: Received 27 October 2014 Accepted 2 November 2014 Available online 3 December 2014
Traumatic aneurysms of intracranial arteries are rare, forming less than 1% of all intracranial arteries. They may be associated with penetrating and non-penetrating trauma. Most cases are associated with fracturing of the skull. Rupture of traumatic aneurysms occur in up to 50% of cases and are typically delayed from days to weeks following the initiating trauma. We report a case of a 22-year-old man who was punched to the head. He was rendered unconscious but recovered and had a GCS of 14 on admission. CT scans showed subarachnoid hemorrhage. An initial angiogram was negative but on day 7 following the incident he was noted to have a 1 mm aneurysm of the posterior inferior cerebellar artery on CT angiogram. On day 9 he collapsed and was found to have new subarachnoid hemorrhage and to have a 4.0 mm 3.7 mm. He did not recover and was declared brain dead on day 12. At autopsy, there was a 4.0 mm aneurysm of the left PICA just after the origin of the artery. Histological examination confirmed the presence of a traumatic false aneurysm in the left PICA. This case study shows sequential radiological imaging with pathologiocal correlation. ß 2014 Elsevier Ireland Ltd. All rights reserved.
Keywords: Aneurysm Traumatic Intracranial False Rupture PICA
1. Introduction Blunt trauma to the head and neck can produce a variety of injuries. Blunt trauma to the neck can cause severe injury to the vertebral and carotid arteries. Blunt trauma to the head can produce more types of injuries based on a variety of mechanisms. Acceleration injuries can produce focal or diffuse injury to the axons and blunt trauma can also cause injury to the intracranial distal portions of the carotid arteries (anterior cerebral arteries) and posterior vessels. Intracranial traumatic aneurysms are extremely rare and are associated with blunt or penetrating injury and most reported cases have been associated with a skull fracture [1–6]. They make up less than 1% of all intracranial aneurysms and are more common in children and males due to increased incidence of trauma [2,3,7,8]. Mao and colleagues found 15 cases following blunt trauma out of 2335 intracranial aneurysms (0.64%) with motor vehicle collisions accounting for 10 cases and falls for the other * Corresponding author at: Division of Anatomical Pathology, The Ottawa Hospital, 501 Smyth Road, Ottawa K1H 8L6, Canada. Tel.: +1 613 737 8899 ex 79812. E-mail address: [email protected] (C.M. Milroy). http://dx.doi.org/10.1016/j.forsciint.2014.11.003 0379-0738/ß 2014 Elsevier Ireland Ltd. All rights reserved.
5 cases [8]. They also had 1 case with penetrating trauma and 4 iatrogenic cases. Aneurysms of the superior and posterior inferior cerebellar arteries have been reported with and without associated skull fracturing [9,10]. The clinical presentation is variable, with subarachnoid hemorrhage (SAH), acute loss of consciousness, seizures, and neurological deficits appearing immediately or months to years later [1–4]. Histologically, traumatic aneurysms have been classified by Burton according to the types of vascular trauma and aneurysms produced, which are true aneurysms, false aneurysms, and mixed or dissecting aneurysms [1]. True aneurysms involve three intact arterial wall layers and demonstrate a partial disruption of the arterial wall leading to weakening and aneurysm formation secondary to flow dynamics. False aneurysms are considered to be the most common histological type associated with head trauma and result from disruption of all three layers of the vessel wall with formation of a contained hematoma surrounded by adventitia and periadventitial tissues and communicating with the vessel lumen. False aneurysms grow faster than true aneurysms, and their risk of re-bleeding is very high. Mixed aneurysm describes rupture of a true aneurysm leading to the formation of a false aneurysm.
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B. Purgina, C.M. Milroy / Forensic Science International 247 (2015) e1–e5
Fig. 1. A conventional catheter angiogram showing no evidence of an aneurysm or fistula.
We report a case of traumatic aneurysm of the left posterior inferior cerebellar artery (PICA) in young man following a punch to the head, without any penetrating injury or skull fracture.
2. Case report A 22-year-old man attempted to break up the fight between two other men and was struck at least once to the head. He collapsed immediately and was unconscious. Initial assessment by paramedics at the scene determined that he had a Glasgow Coma Scale (GCS) score of 3/4 and he required ventilatory support with a bag. His pupils were dilated and deviated to the left. Overall he appeared post-ictal to the paramedics. At the emergency department, he was noted to have a GCS of 14. Abrasions were noted to the left brow, right forehead and there was vomitus in the left ear. Subsequently his GCS fluctuated from 11 to 14 and he was ventilated and admitted to the intensive care unit. Initial CT scan showed diffuse moderate SAH and intraventricular hemorrhage (IVH) as well as mild hydrocephalus. A conventional catheter angiogram showed no evidence of obvious aneurysm or fistula (Fig. 1). No evidence of vasospasm was seen. An admission blood ethanol was 39 mmol/L (177 mg/100 ml). On Day 2, the patient was extubated. Subsequently he had a GCS score of 15, although he complained of headaches and some memory loss. A CT scan done on Day 2 showed slight progression of the hydrocephalus. On Day 7, CT scan of the brain without contrast and CT angiogram of the circle of Willis was performed. There was minimal residual blood in the right occipital horn. Previously documented SAH had completely resolved. The minimal ventricular prominence was unchanged. There was no evidence of infarction seen and no evidence of extra axial collection was seen. CT angiogram performed demonstrated a tiny 1.0 mm aneurysm at the origin of the left PICA (Fig. 2). There was a normal appearance to the rest of the intracranial arteries. There was no other aneurysm or arterio-venous malformation noted. By Day 9 he was fully mobilizing and had left the ward to go to smoke a cigarette, a friend described him as going limp and being unresponsive. Following this collapse, he had a GCS of 3. CT scan was performed which showed that there was new IVH and SAH in the left cerebellopontine angle region and at the level of the foramen magnum. This was in keeping with a ruptured aneurysm of the left PICA. A 4.0 mm 3.7 mm aneurysm of the left PICA was demonstrated (Fig. 3).
A further CT scan conducted on Day 10 showed little change and extensive SAH and IVH remaining. He developed fixed dilated pupils and his condition did not improve. Brain stem death was confirmed on Day 12. The findings at autopsy included were that the brain was markedly swollen, weighing 1700 g, and tonsillar grooving was evident. No contusional damage of the brain parenchyma was identified and there were no focal lesions seen on sectioning of the brain. SAH was most notable around the origin of the left PICA. Examination of the circle of Willis demonstrated a 4.0 mm aneurysm of the left PICA just after the origin of the artery (Fig. 4). The remaining vessels of the circle of Willis appeared normal. Histological examination (Figs. 5 and 6) confirmed the presence of a traumatic false aneurysm in the left PICA. The rupture site was demonstrtaed (Fig. 7). Aneurysmal dilation was composed of adventitial tissue partially surrounding a hematoma (Fig. 8). The distal end of the aneurysm, that is the side opposite the aneurysm mouth, had ruptured. No hemosiderin staining was present and
Fig. 2. CT angiogram performed on day 7 demonstrated a tiny 1.0 mm aneurysm at the origin of the left PICA.
B. Purgina, C.M. Milroy / Forensic Science International 247 (2015) e1–e5
Fig. 3. CT angiogram performed on day 9. There was a 4.0 3.7 mm aneurysm of the left PICA.
Fig. 4. 4.0 mm aneurysm of the left PICA just after the origin of the artery.
Fig. 5. Traumatic false aneurysm in the left PICA (hemotoxylin and eosin).
Fig. 6. Traumatic false aneurysm in the left PICA (Masson trichrome).
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B. Purgina, C.M. Milroy / Forensic Science International 247 (2015) e1–e5
e4
Fig. 7. Traumatic false aneurysm rupture site (Movat stain).
Fig. 9. Corpus callosum necrosis, with hemosiderin and red blood cells identified (a and b). Fig. 8. Aneurysmal dilation with adventitial tissue partially surrounding a hematoma.
there was no evidence of a long-standing aneurysm. The arteries of the circle of Willis showed no underlying abnormality. Neurohistology confirmed the presence of established hypoxic changes throughout the brain with prominent cerebral edema. In the corpus callosum there were areas of necrosis, with hemosiderin and red blood cells identified (Fig. 9a and b). There are obvious axonal retraction balls in these areas. Stains for beta-amyloid precursor protein (b-APP) were positive confirming axonal damage in the corpus callosum. 3. Discussion Traumatic aneurysms are very rare. Most are located near the midline or base of skull, in the region of the circle of Willis, mainly affecting the middle cerebral artery, anterior cerebral artery, or internal carotid artery [1–6]. Less than 10% involve the posterior circulation and are associated with SAH and brain stem ischemia [8]. Approximately 50% of reported cases of traumatic aneurysms undergo delayed rupture, with an average interval 14–21 days [1– 6]. The mortality rate varies between 32–54% in untreated cases and 18–24% after surgical management [3,5]. The majority of traumatic aneurysms have been reported as result of direct vascular injury secondary to skull fracture or penetrating injury [5,11]. Rarely they form as a result of shearing forces causing torsion and overstretching of the vessels of the
arteries at the time of trauma [5,11], though the frequency of the cause of traumatic aneurysms may depend on local factors. A report of 13 cases from Israel involved 7 explosions, 2 gunshot wounds, 2 motor vehicle collisions, one stabbing and on fall from a height [12]. Bell and colleagues reported on 64 military cases [13]. In our patient, blunt craniocervical trauma creating acceleration and deceleration of the cerebellum within the skull injuring the PICA at its origin, explains the formation of a traumatic aneurysm of the left PICA and traumatic axonal injury in the corpus callosum. Traumatic aneurysms should be suspected in the setting of acute neurological deterioration following any type of closed head injury and patients should undergo immediate CT scanning. If the scan demonstrates SAH in a pattern suggestive of aneurysmal SAH (IVH with SAH or posterior fossa SAH), an angiogram usually follows to look for vascular injury [5,11]. CT features suggestive of PICA aneurysm rupture include IVH with hydrocephalus, seen in 90% of cases [11]. It is rare to see SAH at the level of cerebral convexities in ruptured PICA aneurysms [11]. In this case, our patient demonstrated at presentation to hospital fluctuating GCS and initial imaging demonstrated the presence of IVH with hydrocephalus and SAH concentrated around the basal circulation of the brain, typical pattern of rupture PICA aneurysm [9]. Initial catheter angiogram did not reveal the presence of an aneurysm. A week later imaging confirmed complete resolution of the SAH and a CT angiogram demonstrated a newly formed 1.0 mm aneurysm at the origin of the left PICA. Two days later, the aneurysm had enlarged and ruptured causing massive neurologic injury leading to death. At presentation, our patient had a blood
B. Purgina, C.M. Milroy / Forensic Science International 247 (2015) e1–e5
ethanol concentration of 39 mmol/L (177 mg/100 mL). A degree of motor and cognitive in-coordination is expected, however it did not directly contributed to his death. Even though more than 100 cases of traumatic aneurysms are reported in the literature, most are associated with penetrating head injuries and skull fractures. Traumatic aneurysms involving the vertebral artery or the PICA are extremely rare, with only 10 other cases in the literature. Eight of these cases are associated with skull fracture. To the best of our knowledge, this is the only case with imaging demonstrating the evolution of the traumatic aneurysm and pathological correlation. When dealing with aneurysmal bleeding following trauma, one wonders whether a pre-existing berry aneurysm has ruptured due to mechanical damage or arterial hypertension [5]. Sequential imaging in this case proves without a doubt that this is a traumainduced aneurysm. Strictly speaking, the diagnosis of traumatic aneurysms would require proof of their formation after head trauma by comparing pre- and post-traumatic angiographic studies [14]. Other features that are useful to distinguish a traumatic aneurysm from a natural ‘‘berry’’ aneurysm include young male, history of trauma and angiographic features including peripheral location, site away from a branching point, irregular outline of the sac, absence of neck, delayed filling and emptying and location adjacent to the falx edge [15,16]. Traumatic aneurysms are often fragile, prone to rupture and present a challenge for either surgical or endovascular therapy. The goal of managing patients with traumatic aneurysms is early diagnosis and intervention to prevent delayed-onset re-bleeding or other thromboembolic complications.
e5
References [1] C. Burton, F. Velasco, J. Dorman, Traumatic aneurysm of a peripheral cerebral artery: review and case report, J. Neurosurg. 28 (1968) 468–474. [2] B.G. Benoit, G. Wortzman, Traumatic cerebral aneurysms. Clinical features and natural history, J. Neurol. Neurosurg. Psychiatry 36 (1973) 127–138. [3] S. Asari, S. Nakamura, O. Yamada, H. Beck, H. Sugatani, H. Higashi, Traumatic aneurysm of peripheral cerebral arteries, J. Neurosurg. 46 (1977) 795–803. [4] B. Holmes, R.E. Harbaugh, Traumatic intracranial aneurysms: a contemporary review, J. Trauma 35 (1993) 855–860. [5] T. Nishioka, Y. Maeda, Y. Tomogane, A. Nakano, N. Arita, Unexpected delayed rupture of vertebral-posterior inferior cerebellar artery aneurysms following closed head Injury, Acta Neurochir. 144 (2002) 839–845. [6] M.R. Frusco, M.R. Harrigan, Cerebrovascular dissections: a review. Part II: blunt cerebrovascular injury, Neurosurgery 68 (2011) 517–530. [7] T.-C. Yang, Y.-L. Lo, Y.-C. Huang, S.-T. Yang, Traumatic anterior cerebral artery aneurysm following blunt craniofacial trauma, Eur. Neurol. 58 (2007) 239–245. [8] Z. Mao, N. Wang, M. Hussain, et al., Traumatic intracranial aneurysms due to blunt brain injury – a single centre experience, Acta Neurochir. 154 (2012) 2187–2193. [9] H. Yamakawa, Y. Kaku, S. Yoshimura, A. Ohkuma, N. Sakai, Two cases of dissecting aneurysm of the distal posterior inferior cerebellar artery: possible involvement of segmental mediolytic arteriopathy in the pathogenesis, Clin. Neurol. Neurosurg. 107 (2005) 117–122. [10] N. Morard m de Tribolet, Traumatic aneurysm of the posterior inferior cerebellar artery: case report, Neurosurgery 29 (1991) 438–439. [11] W.S. Paiva, A.F. Andrade, H.S. Neto, et al., Traumatic pseudoaneurysm of the superior cerebellar artery, J. Trauma 72 (2011) E115. [12] J.E. Cohen, J.M. Gomori, R. Segal, et al., Results of endovascular treatment of traumatic intracranial aneurysms, Neurosurgery 63 (2008) 476–484. [13] R.S. Bell, A.H. Vo, R. Roberts, et al. Neurosurgery 66 (2010) 66–79. [14] D. Kallmes, G. Lanzino, J.E. Dix, J.E. Dion, H. Do, R.J. Woodcock, N.F. Kassell, Patterns of hemorrhage with ruptured posterior inferior cerebellar artery aneurysms: CT findings in 44 cases, Am. J. Rad. 169 (1997) 1169–1171. [15] F. Quintana, C. Diez, A. Gutierrez, M.L. Diez, O. Austin, A. Vazquez, Traumatic aneurysm of the basilar artery, Am. J. Neuroradiol. 17 (1994) 283–285. [16] K. Opeskin, Traumatic pericallosal artery aneurysm, Am. J. Forensic Med. Pathol. 16 (1995) 11–16.