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Carotid artery hemorrhage resulting from temporal bone fracture
Carotid Artery Hemorrhage Temporal Bone Fracture
Resulting
Theodoros N. Teknos, MD, Michael I? Joseph, MD, CliffA. Robert M. Friedlander, MD, and Alfred L. Weber, MD
(Editorial Comment: The authors describe a harrowing case and reflect on the therapeutic options that may be considered.) Temporal bone fractures represent 22% of all skull fractures and are being recognized more frequently as a result of high-resolution computed tomography (CT).l These fractures are commonly caused by blunt head trauma associated with motor vehicle accidents or falls. The clinical manifestations of temporal bone fractures include hemotympanum, hearing loss, vertigo, facial paralysis, and cerebrospinal fluid otorrhea. 2 Ghoyareb et al2 documented several unusual complications of temporal bone fractures, including abducens palsy, trigeminal paralysis, and aseptic sigmoid sinus thrombosis. Injuries to the petrous carotid artery in temporal bone fracture have not been widely reported in the English literature. This rare case of internal carotid artery injury from temporal bone fracture serves to characterize the clinical presentation of this complication and is the first such report to include CT confirmation of petrous carotid artery rupture.
CASE REPORT A 33-year-old construction worker was brought to the emergency room after falling 30 ft onto the vertex of his head. He was found by the emergency medical technicians at the scene with bilateral fixed and dilated pupils. He was pharmacologically paralyzed and intubated, after cervical spine immoFrom the Departments of Otolaryngology and Radiology, Massachusetts Eye and Ear Infirmary, Harvard Medical School; and the Departments of Neurosurgery and Radiology, Massachusetts General Hospital, Harvard Medical School, Boston MA. Address reprint requests to Theodoros N. Teknos, MD, Department of Otolaryngology, University of Michigan Medical Center, 1500 E Medical Center Dr, Room TC 1904, Ann Arbor, Ml 48103. Copyright o 1997 by W.B. Saunders Company 0196-0709/97/l 805-0009$5.00/O 338
American
Journal
of Otolatyngology,
From
Megerian, MD,
bilization. During the helicopter transfer, it was noted that the patient was profusely bleeding from his left ear. On arrival to the emergency room, the patient’s systolic blood pressure was 80 mm Hg and the bleeding from his left ear had markedly diminished. Initial neurological examination showed bilateral fixed, dilated pupils with trace cornea1 and gag reflexes, and no withdrawal of the extremities to noxious stimuli. The patient was treated with fluids to which his blood pressure responded by increasing to 130/84 mm Hg. Initial relevant laboratory values included a hematocrit of 38.5% and a prothrombin time of 15.5/10.3. A rapid, spiral cranial CT scan showed a large left subdural hematoma near obliteration of the basal cisterns and skull fractures, which extended from the suboccipital region to the vertex including a fracture line through the left temporal bone and carotid canal (Fig 1). Immediately on completion of the CT scan, the patient developed massive bright red otorrhagia from the left ear and epistaxis measuring an estimated 2 L. The Otolaryngology Department was urgently consulted, and the left external auditory canal was promptly and tightly packed with petroleum jelly-impregnated iodoform gauze, controlling the bleeding. The patient’s hematocrit, however, had dropped to 8% as a result of this renewed hemorrhage. At this point, the patient was deemed too unstable for angiography, both hemodynamitally as well as from a neurosurgical standpoint, secondary to impending cerebral herniation. Therefore, he rapidly received O-negative packed red blood cell infusions and was taken directly to the operating room for evacuation of the left subdural hematoma and possible carotid ligation. Burr holes were made and approximately 15 mL of blood was drained from his intracranial cavity. However, at that point in the procedure, the patient became gradually more hemodynamically unstable, culminating with ventricular arrhythmias and ventricular fibrillatory arrest. The wound was rapidly closed, and the patient successfully cardioverted to normal sinus rhythm but remained hemodynamically unstable with a systolic blood pressure of 70 mm Hg. No further bleeding was noted from the ear or nares. The patient was then transported to the intensive care unit, where he remained hemodynamically unstable with intermittent ventricular tachyarrhythmias and in a state of disseminated intravascular coagulopathy. After discussing with the family the severity of the patient’s injuries and current condi-
Vol 18, No 5 (September-October),
1997:
pp 338-340
CAROTID
ARTERY
HEMORRHAGE
FROM
FRACTURE
Fig 1. A CT scan clearly illustrating fractures in the anterior and posterior portions of the carotid canal (large arrow) resulting from a longitudinal temporal bone fracture. Also note the depressed skull fractures (small arrows).
tion, further resuscitation efforts were abandoned and the patient died. DISCUSSION Injuries to the internal carotid artery following blunt head trauma can include dissection, intimal tear, spasm, thrombosis, occlusion, transection, dissecting aneurysm, pseudoaneurysm, arteriovenous fistula, and carotid-cavernous fistula.3*4 These are usually a result of shearing forces on the artery and can occur anywhere along its course. Because of its circumferential encasement in bone, the petrous carotid artery is relatively protected from injury following blunt head trauma. In a review of the world literature dating back to 1935, a total of 115 cases of internal carotid artery aneurysms caused by blunt trauma were reported.5 Of these, only six (5%) were located in the petrous portion, illustrating the protective effect of the bony carotid canal. On the other hand, the internal carotid artery is particularly susceptible to injury at its entrance and exit points from the carotid canal and cavernous sinus. Here, torsion and shearing forces may lead to transection and/or dissection with or without occlusion.3 Underlying vascular disorders, such as cystic medial necrosis, Marfan’s syndrome, fibromuscular dyspla-
339
sia, homocystinuria, and syphilis, have been implicated as predisposing factors to vascular injury in cases of minor trauma.3,6 Laceration of the internal carotid artery, as a complication of temporal bone fractures, has been infrequently reported in the literature. The first reports date back to 1912, in which Rawling7 describes two cases of exsanguinating hemorrhage as a result of skull fractures. Imajo* reports two additional cases and mentions autopsy findings in nine others in which rapid hemorrhagic death occurred due to “typical basal skull fractures.” His patients showed pathological signs of extensive blood loss secondary only to epistaxis and otorrhagia resulting from lacerations of the internal carotid artery. The most comprehensive report on this subject, however, comes from Pollanen et a1.g They report eight cases of transverse fracture of the temporal bone with extension into the carotid canal resulting in exsanguinating otorrhagia. They also confirmed the pathophysiology of the injury by cannulating the carotid artery in the neck, infusing saline, and documenting a brisk egress of fluid through the ear canal. Despite the relative infrequency of this injury, the otolaryngologist or trauma surgeon must be equipped to deal with these emergencies. Much of the treatment schema must be inferred from other lesions presenting as hemorrhage emanating from the petrous carotid artery, namely aneurysms and penetrating trauma. After immobilizing the cervical spine, obtaining an adequate airway, and starting fluid resuscitation, the trauma physician must tamponade the bleeding by tightly packing the external auditory canal with ribbon gauze. If there is bleeding from the nose and mouth, a very tight posterior nasal pack must be placed as well. If despite these efforts the patient continues to bleed profusely, ligation of the common carotid artery is necessary to control life-threatening hemorrhage. When this is done before achieving a normotensive and normovolemic state, the morbidity and mortality rates are exceedingly high (45%).*0 Failure rates are also high as a result of back-bleeding from the intracranial carotid artery.ll This back-bleeding can be controlled by a middle fossa craniotomy for ligation of the internal carotid artery below the take-off of the opthalmic artery.12 On the other hand, if packing can
340
stabilize the hemorrhage so that emergent carotid ligation is not required, detachable balloon embolization may be the treatment of choice. The internal carotid artery is occluded proximal and distal to the laceration by detachable embolization balloons. Although there are no reports of its use in this circumstance, it has been quite successful in the treatment of impending carotid blowout,13 petrous internal carotid artery aneurysms,ll and carotid cavernous fistulas. There have been no studies to date comparing surgical ligation to endovascular balloon occlusion in terms of long-term efficacy, morbidity, or mortality.ll This case represents an interesting variation on the typical presentation of patients with carotid injury caused by temporal bone fractures. Under most circumstances, these patients die before reaching the emergency ward from rapid hemorrhagic death or complications of intracranial trauma. In this case, however, the patient presented to the emergency ward with what was likely a carotid arterial bleed in the form of otorrhagia. Because of the extent of the head injury, this otorrhagia was initially considered to be simply a consequence of longitudinal temporal bone fracture and not a manifestation of intratemporal carotid artery rupture. However, when the patient was in the CT scanner, the bleeding became massive and ultimately may have contributed to the patient’s death. It is likely that a temporarily tamponaded carotid artery rebled as a result of blood pressure elevation from successful fluid resuscitation. In light of this case, it is imperative that otorrhagia beyond the minimal amount typically encountered in longitudinal temporal bone fractures be considered a potentially life-threatening physical finding. Prompt angiography and balloon embolization of the petrous carotid artery can be a life-saving maneuver in such cases. Because
TEKNOS
ET AL
of the nature of these injuries however, CT of the head should be performed first, if possible, to rule out expanding subdural or epidural hematomas. In summary, we present an unusual vascular complication of temporal bone fracture. The literature was reviewed, highlighting the rarity of this condition and the importance of immediate aural tamponade. Finally, definitive treatment options were introduced and their clinical utility reviewed. REFERENCES 1. Cannon CR, Jahrsdoerfer RA: Temporal bone fractures. Arch Otolaryngol 109:285-288, 1983 2. Ghoyar BY, Yeakley JW, Hall JW, Jones BE: Unusual complications of temporal bone fractures. Arch Otolarygo1 Head and Neck Surg 113:749-753,1987 3. Goodwin JR, Johnson MH: Carotid injury secondary to blunt head trauma: Case report. J Trauma 37:x19-122, 1994 4. Anson J, Crowell RM: Cervicocranial arterial dissection. Neurosurgery 29:89-96,199l 5. Fox JL: Associated conditions II, in Fox JL (ed): Intracranial Aneurysms, vol 1. New York, NY, SpringerVerlag, 1983, pp 423-431 6. O’Sullivan RM, Robertson WD, Nugent RA, et al: Supraclinoid carotid artery dissection following unusual trauma. AJNRAm JNeuroradiol ll:ll50-1152,199O 7. Rawling LB: Fracture of skull, in The Surgery of the Skull and Brain. London, United Kingdom, Oxford Medical Press, 1912, pp 68-124 8. Imajo T: Rapid hemorrhagic death due to basal skull fracture. Am J Forensic Med Path01 9:271-272,1988 9. Pollanen MS, Deck JH, Blenkinsop B, Farkas EM: Fracture of temporal bone with exsanguination: Pathology and mechanism. Can J Neurol Sci 19:196-200,1992 10. Miller JD, Jewad K, Jennett B: Safety of carotid ligation and its role in the management of intracranial aneurysms. J Neurol Neurosurg Psychiatry 40:64-72, 1977 11. Constantino PD, Russell E, Reisch D, et al: Ruptured petrous carotid aneurysm presenting with otorrhagia and epistaxis. Am J Otol12:378-383,199l 12. Kleid MS, Millar HS: Internal carotid artery epistaxis. Otolaryngol Head Neck Surg 9:480-486,1986 13. Zimmerman MC, Mickel RA, Kessler DJ, et al: Treatment of impending carotid rupture with detachable balloon embolization. Arch Otolaryngol Head Neck Surg 113:1169-1175,1987
Resulting
Theodoros N. Teknos, MD, Michael I? Joseph, MD, CliffA. Robert M. Friedlander, MD, and Alfred L. Weber, MD
(Editorial Comment: The authors describe a harrowing case and reflect on the therapeutic options that may be considered.) Temporal bone fractures represent 22% of all skull fractures and are being recognized more frequently as a result of high-resolution computed tomography (CT).l These fractures are commonly caused by blunt head trauma associated with motor vehicle accidents or falls. The clinical manifestations of temporal bone fractures include hemotympanum, hearing loss, vertigo, facial paralysis, and cerebrospinal fluid otorrhea. 2 Ghoyareb et al2 documented several unusual complications of temporal bone fractures, including abducens palsy, trigeminal paralysis, and aseptic sigmoid sinus thrombosis. Injuries to the petrous carotid artery in temporal bone fracture have not been widely reported in the English literature. This rare case of internal carotid artery injury from temporal bone fracture serves to characterize the clinical presentation of this complication and is the first such report to include CT confirmation of petrous carotid artery rupture.
CASE REPORT A 33-year-old construction worker was brought to the emergency room after falling 30 ft onto the vertex of his head. He was found by the emergency medical technicians at the scene with bilateral fixed and dilated pupils. He was pharmacologically paralyzed and intubated, after cervical spine immoFrom the Departments of Otolaryngology and Radiology, Massachusetts Eye and Ear Infirmary, Harvard Medical School; and the Departments of Neurosurgery and Radiology, Massachusetts General Hospital, Harvard Medical School, Boston MA. Address reprint requests to Theodoros N. Teknos, MD, Department of Otolaryngology, University of Michigan Medical Center, 1500 E Medical Center Dr, Room TC 1904, Ann Arbor, Ml 48103. Copyright o 1997 by W.B. Saunders Company 0196-0709/97/l 805-0009$5.00/O 338
American
Journal
of Otolatyngology,
From
Megerian, MD,
bilization. During the helicopter transfer, it was noted that the patient was profusely bleeding from his left ear. On arrival to the emergency room, the patient’s systolic blood pressure was 80 mm Hg and the bleeding from his left ear had markedly diminished. Initial neurological examination showed bilateral fixed, dilated pupils with trace cornea1 and gag reflexes, and no withdrawal of the extremities to noxious stimuli. The patient was treated with fluids to which his blood pressure responded by increasing to 130/84 mm Hg. Initial relevant laboratory values included a hematocrit of 38.5% and a prothrombin time of 15.5/10.3. A rapid, spiral cranial CT scan showed a large left subdural hematoma near obliteration of the basal cisterns and skull fractures, which extended from the suboccipital region to the vertex including a fracture line through the left temporal bone and carotid canal (Fig 1). Immediately on completion of the CT scan, the patient developed massive bright red otorrhagia from the left ear and epistaxis measuring an estimated 2 L. The Otolaryngology Department was urgently consulted, and the left external auditory canal was promptly and tightly packed with petroleum jelly-impregnated iodoform gauze, controlling the bleeding. The patient’s hematocrit, however, had dropped to 8% as a result of this renewed hemorrhage. At this point, the patient was deemed too unstable for angiography, both hemodynamitally as well as from a neurosurgical standpoint, secondary to impending cerebral herniation. Therefore, he rapidly received O-negative packed red blood cell infusions and was taken directly to the operating room for evacuation of the left subdural hematoma and possible carotid ligation. Burr holes were made and approximately 15 mL of blood was drained from his intracranial cavity. However, at that point in the procedure, the patient became gradually more hemodynamically unstable, culminating with ventricular arrhythmias and ventricular fibrillatory arrest. The wound was rapidly closed, and the patient successfully cardioverted to normal sinus rhythm but remained hemodynamically unstable with a systolic blood pressure of 70 mm Hg. No further bleeding was noted from the ear or nares. The patient was then transported to the intensive care unit, where he remained hemodynamically unstable with intermittent ventricular tachyarrhythmias and in a state of disseminated intravascular coagulopathy. After discussing with the family the severity of the patient’s injuries and current condi-
Vol 18, No 5 (September-October),
1997:
pp 338-340
CAROTID
ARTERY
HEMORRHAGE
FROM
FRACTURE
Fig 1. A CT scan clearly illustrating fractures in the anterior and posterior portions of the carotid canal (large arrow) resulting from a longitudinal temporal bone fracture. Also note the depressed skull fractures (small arrows).
tion, further resuscitation efforts were abandoned and the patient died. DISCUSSION Injuries to the internal carotid artery following blunt head trauma can include dissection, intimal tear, spasm, thrombosis, occlusion, transection, dissecting aneurysm, pseudoaneurysm, arteriovenous fistula, and carotid-cavernous fistula.3*4 These are usually a result of shearing forces on the artery and can occur anywhere along its course. Because of its circumferential encasement in bone, the petrous carotid artery is relatively protected from injury following blunt head trauma. In a review of the world literature dating back to 1935, a total of 115 cases of internal carotid artery aneurysms caused by blunt trauma were reported.5 Of these, only six (5%) were located in the petrous portion, illustrating the protective effect of the bony carotid canal. On the other hand, the internal carotid artery is particularly susceptible to injury at its entrance and exit points from the carotid canal and cavernous sinus. Here, torsion and shearing forces may lead to transection and/or dissection with or without occlusion.3 Underlying vascular disorders, such as cystic medial necrosis, Marfan’s syndrome, fibromuscular dyspla-
339
sia, homocystinuria, and syphilis, have been implicated as predisposing factors to vascular injury in cases of minor trauma.3,6 Laceration of the internal carotid artery, as a complication of temporal bone fractures, has been infrequently reported in the literature. The first reports date back to 1912, in which Rawling7 describes two cases of exsanguinating hemorrhage as a result of skull fractures. Imajo* reports two additional cases and mentions autopsy findings in nine others in which rapid hemorrhagic death occurred due to “typical basal skull fractures.” His patients showed pathological signs of extensive blood loss secondary only to epistaxis and otorrhagia resulting from lacerations of the internal carotid artery. The most comprehensive report on this subject, however, comes from Pollanen et a1.g They report eight cases of transverse fracture of the temporal bone with extension into the carotid canal resulting in exsanguinating otorrhagia. They also confirmed the pathophysiology of the injury by cannulating the carotid artery in the neck, infusing saline, and documenting a brisk egress of fluid through the ear canal. Despite the relative infrequency of this injury, the otolaryngologist or trauma surgeon must be equipped to deal with these emergencies. Much of the treatment schema must be inferred from other lesions presenting as hemorrhage emanating from the petrous carotid artery, namely aneurysms and penetrating trauma. After immobilizing the cervical spine, obtaining an adequate airway, and starting fluid resuscitation, the trauma physician must tamponade the bleeding by tightly packing the external auditory canal with ribbon gauze. If there is bleeding from the nose and mouth, a very tight posterior nasal pack must be placed as well. If despite these efforts the patient continues to bleed profusely, ligation of the common carotid artery is necessary to control life-threatening hemorrhage. When this is done before achieving a normotensive and normovolemic state, the morbidity and mortality rates are exceedingly high (45%).*0 Failure rates are also high as a result of back-bleeding from the intracranial carotid artery.ll This back-bleeding can be controlled by a middle fossa craniotomy for ligation of the internal carotid artery below the take-off of the opthalmic artery.12 On the other hand, if packing can
340
stabilize the hemorrhage so that emergent carotid ligation is not required, detachable balloon embolization may be the treatment of choice. The internal carotid artery is occluded proximal and distal to the laceration by detachable embolization balloons. Although there are no reports of its use in this circumstance, it has been quite successful in the treatment of impending carotid blowout,13 petrous internal carotid artery aneurysms,ll and carotid cavernous fistulas. There have been no studies to date comparing surgical ligation to endovascular balloon occlusion in terms of long-term efficacy, morbidity, or mortality.ll This case represents an interesting variation on the typical presentation of patients with carotid injury caused by temporal bone fractures. Under most circumstances, these patients die before reaching the emergency ward from rapid hemorrhagic death or complications of intracranial trauma. In this case, however, the patient presented to the emergency ward with what was likely a carotid arterial bleed in the form of otorrhagia. Because of the extent of the head injury, this otorrhagia was initially considered to be simply a consequence of longitudinal temporal bone fracture and not a manifestation of intratemporal carotid artery rupture. However, when the patient was in the CT scanner, the bleeding became massive and ultimately may have contributed to the patient’s death. It is likely that a temporarily tamponaded carotid artery rebled as a result of blood pressure elevation from successful fluid resuscitation. In light of this case, it is imperative that otorrhagia beyond the minimal amount typically encountered in longitudinal temporal bone fractures be considered a potentially life-threatening physical finding. Prompt angiography and balloon embolization of the petrous carotid artery can be a life-saving maneuver in such cases. Because
TEKNOS
ET AL
of the nature of these injuries however, CT of the head should be performed first, if possible, to rule out expanding subdural or epidural hematomas. In summary, we present an unusual vascular complication of temporal bone fracture. The literature was reviewed, highlighting the rarity of this condition and the importance of immediate aural tamponade. Finally, definitive treatment options were introduced and their clinical utility reviewed. REFERENCES 1. Cannon CR, Jahrsdoerfer RA: Temporal bone fractures. Arch Otolaryngol 109:285-288, 1983 2. Ghoyar BY, Yeakley JW, Hall JW, Jones BE: Unusual complications of temporal bone fractures. Arch Otolarygo1 Head and Neck Surg 113:749-753,1987 3. Goodwin JR, Johnson MH: Carotid injury secondary to blunt head trauma: Case report. J Trauma 37:x19-122, 1994 4. Anson J, Crowell RM: Cervicocranial arterial dissection. Neurosurgery 29:89-96,199l 5. Fox JL: Associated conditions II, in Fox JL (ed): Intracranial Aneurysms, vol 1. New York, NY, SpringerVerlag, 1983, pp 423-431 6. O’Sullivan RM, Robertson WD, Nugent RA, et al: Supraclinoid carotid artery dissection following unusual trauma. AJNRAm JNeuroradiol ll:ll50-1152,199O 7. Rawling LB: Fracture of skull, in The Surgery of the Skull and Brain. London, United Kingdom, Oxford Medical Press, 1912, pp 68-124 8. Imajo T: Rapid hemorrhagic death due to basal skull fracture. Am J Forensic Med Path01 9:271-272,1988 9. Pollanen MS, Deck JH, Blenkinsop B, Farkas EM: Fracture of temporal bone with exsanguination: Pathology and mechanism. Can J Neurol Sci 19:196-200,1992 10. Miller JD, Jewad K, Jennett B: Safety of carotid ligation and its role in the management of intracranial aneurysms. J Neurol Neurosurg Psychiatry 40:64-72, 1977 11. Constantino PD, Russell E, Reisch D, et al: Ruptured petrous carotid aneurysm presenting with otorrhagia and epistaxis. Am J Otol12:378-383,199l 12. Kleid MS, Millar HS: Internal carotid artery epistaxis. Otolaryngol Head Neck Surg 9:480-486,1986 13. Zimmerman MC, Mickel RA, Kessler DJ, et al: Treatment of impending carotid rupture with detachable balloon embolization. Arch Otolaryngol Head Neck Surg 113:1169-1175,1987