- Email: [email protected]
Blunt cerebrovascular injuries in the child
The American Journal of Surgery (2012) 204, 7–10
Clinical Science
Blunt cerebrovascular injuries in the child Teresa S. Jones, M.D.a, Clay Cothren Burlew, M.D.a,*, Lucy Z. Kornblith, M.D.a, Walter L. Biffl, M.D.a, David A. Partrick, M.D.b, Jeffrey L. Johnson, M.D.a, Carlton C. Barnett, M.D.a, Denis D. Bensard, M.D.a, Ernest E. Moore, M.D.a a
Department of Surgery, Denver Health Medical Center, Denver, CO, USA; bThe Children’s Hospital, Denver, CO, USA KEYWORDS: Carotid injury; Vertebral injury; Blunt cerebrovascular injury; Trauma; Stroke; Pediatric; Children
Abstract BACKGROUND: Although blunt cerebrovascular injuries (BCVIs) are a well-recognized sequela of trauma in adults, there have been few reports in children. The investigators questioned whether adult screening protocols are appropriate in the pediatric population. The purpose of this study was to describe the incidence, injury patterns, and stroke rates of pediatric patients sustaining BCVIs. METHODS: Pediatric patients (aged ⱕ 18 years) diagnosed with BCVIs at a regional level I trauma center and a pediatric level I trauma center since 1996 were reviewed. RESULTS: Forty-five patients sustained BCVIs (60% male; mean age, 13 ⫾ .7 years; mean Injury Severity Score, 23 ⫾ 2). Three patients exsanguinated, and 10 presented with stroke; neurologic changes occurred 17 ⫾ 6 hours after injury (range, 1–72 hours). Screening indications were present in 30%. Thirty-two asymptomatic patients were diagnosed. All but 1 received antithrombotic agents; 1 patient had neurologic deterioration despite heparinization. Comparing asymptomatic patients with those with stroke, there was a significant difference in age (15 vs 11 years). CONCLUSIONS: More than two-thirds of patients presenting with stroke did not have screening indications according to adult protocols. With the availability of noninvasive diagnostic imaging such as computed tomographic angiography, broader screening guidelines for children should be instituted. © 2012 Elsevier Inc. All rights reserved.
Before 1980, only 96 cases of blunt carotid injuries were reported in the literature.1 With the recognition of these injuries and their associated potential for devastating neurologic sequelae, screening protocols were introduced to identify asymptomatic patients. As a result, the diagnosed incidence of blunt cerebrovascular injuries (BCVIs) increased to 1% in all patients with blunt trauma and as high as 2.7% in those with Injury Severity Scores ⬎ 16.2–5 BCVIs are now a well-recognized sequela of trauma in the adult population, but there have been few reports in chil-
Presented at the 63rd Annual Meeting of the Southwestern Surgical Congress, Ko Olina, Hawaii. * Corresponding author: Tel.: 303-436-6558; fax: 303-436-6572. E-mail address: [email protected] Manuscript received May 20, 2011; revised manuscript July 25, 2011
0002-9610/$ - see front matter © 2012 Elsevier Inc. All rights reserved. doi:10.1016/j.amjsurg.2011.07.015
dren. In 1999, Lew et al6 reported the largest cohort of pediatric BCVIs to date, on the basis of the National Pediatric Trauma Registry; their review identified an incidence of blunt carotid injuries of .03% (15 of 57,659 patients with blunt trauma). The authors speculated that this low incidence could be related to either underdiagnosis of injuries or actual decreased incidence compared with adults; a decrease in incidence could be due to innate, protective physiologic differences, namely, the lack of atherosclerotic disease and increased vascular elasticity in children. With few pediatric cases of BCVIs, management is currently based on isolated case reports, and the identification of injuries is often after neurologic deficits are discovered. There are no screening recommendations for BCVIs in children. The most recent Eastern Association for the Surgery of Trauma consensus guidelines support standard adult
8
The American Journal of Surgery, Vol 204, No 1, July 2012
screening triggers in the pediatric population.2 We questioned whether this screening protocol is appropriate on the basis of current epidemiology. The purpose of this study was to describe the incidence, injury patterns, presentation, and stroke rates of pediatric patients sustaining BCVIs.
Results
Methods All pediatric patients (aged ⱕ 18 years) diagnosed with BCVIs at our regional level I trauma center and pediatric level I trauma center since 1996 were reviewed. Denver Health Medical Center is a state-certified and American College of Surgeons–verified level I regional trauma center and an integral teaching facility of the University of Colorado School of Medicine. The Children’s Hospital is a level I regional pediatric trauma center and teaching facility of the University of Colorado. During the 1st portion of the study period, our screening test for patients at risk for BCVIs was 4-vessel cerebrovascular angiography; since 2007, multislice computed tomographic angiography (CTA) has become the preferred imaging modality as confidence in this test has been established.3–12 In patients who are candidates for antithrombotic therapy, screening is performed as soon as possible after evaluation of life-threatening injuries. Patients’ injuries were classified according to the Denver grading scale (Table 1).13 Once a BCVI was identified, either a carotid artery injury or a vertebral artery injury, antithrombotic therapy was started unless contraindicated by an associated injury at risk for bleeding. Initially, standard heparinization protocols were used, but because of a moderate incidence of bleeding in patients with multisystem trauma, the protocol was modified.14 The current anticoagulation protocol involves initiating systemic heparin as a continuous infusion of 15 U/kg/h, without a loading dose. The dosage was adjusted thereafter to achieve a partial thromboplastin time of 40 to 50 seconds. Alternatively, antiplatelet agents (aspirin 325 mg/d and/or clopidogrel 75 mg/d) were administered at the discretion of the attending surgeon. Statistical analysis was performed using SAS for Windows (SAS Institute Inc, Cary, NC). The Colorado Multi-Institutional Review Board approved this study.
Table 1
Denver grading scale for BCVI
Grade
Description
I
Irregularity of the vessel wall or a dissection or intramural hematoma with ⬍25% luminal stenosis Intraluminal thrombus or raised intimal flap is visualized, or dissection or intramural hematoma with ⱖ25% luminal narrowing Pseudoaneurysm Vessel occlusion Vessel transection
II
III IV V
From January 1996 to January 2010, 14,991 pediatric patients were admitted for blunt trauma, and 45 patients (.3%) were diagnosed with BCVIs. The majority (60%) were male, with a mean age of 13 ⫾ .7 years (range, 1.5–18 years) and a mean Injury Severity Score of 23 ⫾ 2. Thirtyone patients had carotid injuries, 11 had vertebral injuries, and 3 had both. Carotid injuries included 12 grade I injuries, 9 grade II injuries, 9 grade III injuries, 8 grade IV injuries, and 7 grade V injuries. Vertebral injuries included 6 grade I injuries, 2 grade II injuries, no grade III injuries, 8 grade IV injuries, 1 grade V injury. Mechanisms of injury included motor vehicle collisions (n ⫽ 24), automobile-pedestrian accidents (n ⫽ 9), direct blows to the neck (n ⫽ 2), falls (n ⫽ 2), motorcycle or snowmobile collisions (n ⫽ 2), assaults (n ⫽ 2), a snowboard accident (n ⫽ 1), a hanging (n ⫽ 1), and other mechanisms (n ⫽ 2). Associated injuries included cervical spine injuries (n ⫽ 19 [40%]), traumatic brain injuries (n ⫽ 16 [34%]), midface or mandible fractures (n ⫽ 9 [19%]), thoracic injuries (n ⫽ 16 [34%]), abdominal injuries (n ⫽ 14 [30%]), pelvic fractures (n ⫽ 11 [23%]), and extremity fractures (n ⫽ 15 [32%]). Mean intensive care unit and hospital lengths of stay were 14 ⫾ 1 and 18 ⫾ 1 days, respectively. Overall mortality was 9%. Thirty-two asymptomatic patients were diagnosed with BCVIs; 23 of these 32 patients (72%) met screening criteria according to adult protocols. Screening indications included cervical spine fractures (13 patients), skull fractures involving the carotid canal (3 patients), traumatic brain injuries or diffuse axonal injuries (3 patients), LeForte II or III fractures (3 patients), and mechanism of injury (1 patient). All but 1 of the asymptomatic patients were treated with antithrombotic agents, and 97% had no neurologic complications. One patient, who was a Jehovah’s Witness, with a grade IV injury (occlusion) of her right carotid artery and a grade II/III injury (⬎25% luminal narrowing/pseudoaneurysm) of her left carotid initially had a transient ischemic attack; for the first 48 hours, she was subtherapeutic on a heparin drip, but by hospital day 3, she was therapeutic. She developed neurologic symptoms with altered mental status and agitation early on day 4 and progressed to hemiplegia despite heparinization. Progressive luminal narrowing with high-grade stenosis was demonstrated on repeat CTA during the evaluation of the patient’s neurologic change, and she underwent carotid stenting of the left carotid artery. Three patients exsanguinated from carotid artery injuries. Ten patients (22%) presented with signs or symptoms of neurologic ischemia before diagnosis, with neurologic changes occurring a mean of 17 ⫾ 6 hours after injury (range, 1–72 hours); 91% of patients with stroke had carotid injuries as the etiology. Current adult BCVI screening indications for those patients with stroke were present in just 3 of the 10 patients (1 with marked soft tissue swelling, C-1 fracture, C-2 fracture). Of these 3 patients, 1 did not present with neurologic symptoms and did undergo screening CTA with a diagnosed grade I carotid injury; the patient could not
T.S. Jones et al.
Blunt cerebrovascular injuries in the child
be anticoagulated because of the traumatic brain injury and subsequently sustained a stroke approximately 72 hours after the injury. Five patients had major injuries that included skull fractures not involving the carotid canal (3 patients), mandible fracture (1 patient), and traumatic brain injury (1 patient). Two patients had no other identified injuries. Comparing asymptomatic patients with those with stroke, there was a significant difference in age (asymptomatic 15 ⫾ .5 years vs stroke 11 ⫾ 1.8 years). Twelve patients (27%) with BCVIs were ⱕ12 years old, and only 5 of these were asymptomatic at diagnosis. Thirty-one patients were diagnosed via arteriography, and 12 patients were diagnosed with CTA. Two patients who exsanguinated were diagnosed before imaging was completed. Mean creatinine at the time of admission was .7 mg/dL, and after 48 hours, mean creatinine was .6 mg/dL. One patient sustained acute kidney injury after posttraumatic nephrectomy. No patient required dialysis during hospitalization. One patient, who had bilateral occlusion of her vertebral arteries, developed gastrointestinal bleeding on hospital day 12, 1 week after the initiation of a heparin drip. She was noted to have gastric ulcerations in her stomach during endoscopy for percutaneous gastrostomy tube placement on hospital day 5. Her heparin drip was discontinued, and she required a total of 3 U of packed red blood cells. She was started on low–molecular weight heparin for prophylaxis and did not develop any neurologic symptoms.
Comments BCVIs are believed to be a rare phenomenon in the pediatric population. The most recent Eastern Association for the Surgery of Trauma consensus guidelines support standard adult screening triggers for children.2 Upon review of the current literature, however, there is a paucity of data to suggest these are appropriate guidelines for the pediatric age range. In our evaluation, 45 children were found to have BCVIs, with an incidence of .3% of all blunt pediatric trauma admissions. This incidence is significantly higher than previous retrospective reviews for pediatric populations,6 likely because of an increased awareness and aggressive screening at our institution. Only 72% of asymptomatic pediatric patients with BCVIs had screening criteria according to adult protocols, and of those presenting with neurologic findings, more than two thirds did not have screening indications. Screening criteria that could be modified for children include injury pattern and mechanism. In addition to the adult screening criteria, the incidence of nonbasilar skull fracture and chest trauma was particularly high among symptomatic patients. Among asymptomatic patients, nonbasilar skull fracture, chest trauma, and traumatic brain injury were the most common. Previous studies have demonstrated a 4-fold to 8-fold risk for BCVI in children and adults with any chest trauma; isolated clavicle fractures are
9 associated with an 8-fold increase in BCVI risk.6,15 In addition to high-velocity mechanisms such as motor vehicle collisions and automobile-pedestrian accidents, low-impact trauma including short-distance falls and direct blows were also implicated in several patients with carotid injuries in our population. As indicated in previous case reports, these mechanisms, however benign sounding, can result in BCVIs, often with significant neurologic deficits before presentation.16 –18 For all age groups, it is important to include mechanism as a screening trigger in addition to clinical presentation. All of our patients were involved in either high-mechanism trauma (motor vehicle collisions, automobile-pedestrian accidents, motorcycle collisions, falls, and snowboarding collisions in 84%), or they sustained direct trauma to the neck (assault and hanging in 16%). There is a proven reduction in stroke rate for both carotid and vertebral artery injuries with antithrombotic treatment.19,20 Therefore, screening during the asymptomatic period before the onset of stroke is critical. CTA has been shown to be sensitive and specific for neck and extremity pediatric trauma,21 but there are concerns that increased screening would result in an increased radiation risk for more children, and that magnetic resonance angiography (MRA) is a better choice for children. Several studies comparing CTA with MRA for BCVI have shown lower sensitivity and specificity for MRA (50%–75% and 47%– 67%, respectively),22 so MRA has not been advocated as an optimal screening modality, but there have been no recent reports comparing the efficacy of MRA with that of CTA. There was a documented latent period in these patients, which could afford time for diagnosis and treatment. Of the initially asymptomatic patients with diagnosed BCVI, 1 patient had neurologic changes after heparinization and was subsequently treated with carotid stenting. With only 1 complication related to antithrombotic therapy, treatment to prevent stroke appears safe. There were several limitations of this study. This was a retrospective review of our data, not a randomized controlled trial. Many patients were not compliant with follow-up imaging, so the long-term histories of these injuries are unknown. Finally, the type of antithrombotic treatment (heparin vs antiplatelet agents) was individualized at the surgeon’s discretion. Before the development of screening guidelines, there was a BCVI rate of .08% to .17% in all blunt trauma admissions.14 After implementation of the screening protocols, 39% to 41% of patients who had 1 of the screening factors had identified BCVIs.23 Once thought to be a rare occurrence, BCVIs are now diagnosed in ⬎1% of adult patients with blunt trauma. The incidence of BCVIs in children is significantly higher than previously suspected, and historically patients have presented after neurologic deterioration. With effective stroke prevention in children with antithrombotic agents, early screening for BCVIs and associated treatment should be pursued. With the increased availability and ease of noninvasive imaging with CTA, in
10
The American Journal of Surgery, Vol 204, No 1, July 2012
addition to the devastating morbidity associated with missed injuries, broader screening guidelines for children should be instituted.
11. Utter GH, Hollingworth W, Hallam DK, et al. Sixteen-slice CT angiography in patients with suspected blunt carotid and vertebral artery injuries. J Am Coll Surg 2006;203:838 – 48. 12. Biffl WL, Egglin T, Benedetto B, et al. Sixteen-slice computed tomographic angiography is a reliable noninvasive screening test for clinically significant blunt cerebrovascular injuries. J Trauma 2006;60: 745–51. 13. Biffl WL, Moore EE, Offner PJ, et al. Blunt carotid arterial injuries: implications of a new grading scale. J Trauma 1999;47:845–53. 14. Biffl WL, Moore EE, Ryu RK, et al. The unrecognized epidemic of blunt carotid arterial injuries: early diagnosis improves neurologic outcome. Ann Surg 1998;228:462–70. 15. Parikh AA, Luchette FA, Valente JF, et al. Blunt carotid artery injuries. J Am Coll Surg 1997;185:80 – 6. 16. Cuff RF, Thomas JH. Pediatric blunt carotid injury from low impact trauma: a case report and review of the literature. J Trauma 2005;58: 620 –3. 17. Payton TF, Siddiqui KM, Sole DP, et al. Traumatic dissection of the internal carotid artery. Pediatr Emerg Care 2004;20:27–9. 18. Lin JJ, Chou ML, Lin KL, et al. Cerebral infarct secondary to traumatic carotid artery dissection. Pediatr Emerg Care 2007;23: 166 – 8. 19. Cothren CC, Biffl WL, Moore EE, et al. Treatment for blunt cerebrovascular injuries: Equivalence of anticoagulation and antiplatelet agents. Arch Surg 2009;44:685–90. 20. Miller PR, Fabian TC, Croce MA, et al. Prospective screening for blunt cerebrovascular injuries: analysis of diagnostic modalities and outcomes. Ann Surg 2002;236:386 –93. 21. Hohan AR, Lineen EB, Perez EA, et al. Value of computed tomographic angiography in neck and extremity pediatric vascular trauma. J Pediatr Surg 2009;44:1236 – 42. 22. Biffl WL. Diagnosis of blunt cerebrovascular injuries. Curr Opin Crit Care 2003;9:530 – 4. 23. Cothren CC, Moore EE, Ray CE, et al. Screening for blunt cerebrovascular injuries is cost effective. Am J Surg 2005;190:845–9.
References 1. Krajweski LP, Hertzer NR. Blunt carotid artery trauma: report of two cases and review of the literature. Ann Surg 1980;191:341– 6. 2. Bromberg WJ, Collier BC, Diebel LN, et al. Blunt cerebrovascular injury practice management guidelines: the Eastern Association for the Surgery of Trauma. J Trauma 2010;68:471–7. 3. Biffl WL, Cothren CC, Moore EE, et al. Western Trauma Association critical decisions in trauma: screening for and treatment of blunt cerebrovascular injuries. J Trauma 2009;67:1150 –3. 4. Burlew CC, Biffl WL. Blunt cerebrovascular trauma. Curr Opin Crit Care 2010;16:587–95. 5. Burlew CC, Biffl WL. Imaging for blunt carotid and vertebral artery injuries. Surg Clin North Am 2011;91:217–31. 6. Lew SM, Frumiento C, Wald SL. Pediatric blunt carotid injury: a review of the National Pediatric Trauma Registry. Pediatr Neurosurg 1999;l30:239 – 44. 7. Berne JD, Reuland KS, Villarreal DH, et al. Sixteen-slice multidetector computed tomographic angiography improves the accuracy of screening for blunt cerebrovascular injury. J Trauma 2006;60:1204 –9. 8. Bub LD, Hollingworth W, Jarvik JG, et al. Screening for blunt cerebrovascular injury: Evaluating the accuracy of multidetector computed tomographic angiography. J Trauma 2005;59:691–7. 9. Schneidereit NP, Simons R, Nicolau S, et al. Utility of screening for blunt vascular neck injuries with computed tomographic angiography. J Trauma 2006;60:209 –16. 10. Eastman AL, Chason DP, Perez CL, et al. Computed tomographic angiography for the diagnosis of blunt cervical vascular injury: is it ready for primetime? J Trauma 2006;60:925–9.
Clinical Science
Blunt cerebrovascular injuries in the child Teresa S. Jones, M.D.a, Clay Cothren Burlew, M.D.a,*, Lucy Z. Kornblith, M.D.a, Walter L. Biffl, M.D.a, David A. Partrick, M.D.b, Jeffrey L. Johnson, M.D.a, Carlton C. Barnett, M.D.a, Denis D. Bensard, M.D.a, Ernest E. Moore, M.D.a a
Department of Surgery, Denver Health Medical Center, Denver, CO, USA; bThe Children’s Hospital, Denver, CO, USA KEYWORDS: Carotid injury; Vertebral injury; Blunt cerebrovascular injury; Trauma; Stroke; Pediatric; Children
Abstract BACKGROUND: Although blunt cerebrovascular injuries (BCVIs) are a well-recognized sequela of trauma in adults, there have been few reports in children. The investigators questioned whether adult screening protocols are appropriate in the pediatric population. The purpose of this study was to describe the incidence, injury patterns, and stroke rates of pediatric patients sustaining BCVIs. METHODS: Pediatric patients (aged ⱕ 18 years) diagnosed with BCVIs at a regional level I trauma center and a pediatric level I trauma center since 1996 were reviewed. RESULTS: Forty-five patients sustained BCVIs (60% male; mean age, 13 ⫾ .7 years; mean Injury Severity Score, 23 ⫾ 2). Three patients exsanguinated, and 10 presented with stroke; neurologic changes occurred 17 ⫾ 6 hours after injury (range, 1–72 hours). Screening indications were present in 30%. Thirty-two asymptomatic patients were diagnosed. All but 1 received antithrombotic agents; 1 patient had neurologic deterioration despite heparinization. Comparing asymptomatic patients with those with stroke, there was a significant difference in age (15 vs 11 years). CONCLUSIONS: More than two-thirds of patients presenting with stroke did not have screening indications according to adult protocols. With the availability of noninvasive diagnostic imaging such as computed tomographic angiography, broader screening guidelines for children should be instituted. © 2012 Elsevier Inc. All rights reserved.
Before 1980, only 96 cases of blunt carotid injuries were reported in the literature.1 With the recognition of these injuries and their associated potential for devastating neurologic sequelae, screening protocols were introduced to identify asymptomatic patients. As a result, the diagnosed incidence of blunt cerebrovascular injuries (BCVIs) increased to 1% in all patients with blunt trauma and as high as 2.7% in those with Injury Severity Scores ⬎ 16.2–5 BCVIs are now a well-recognized sequela of trauma in the adult population, but there have been few reports in chil-
Presented at the 63rd Annual Meeting of the Southwestern Surgical Congress, Ko Olina, Hawaii. * Corresponding author: Tel.: 303-436-6558; fax: 303-436-6572. E-mail address: [email protected] Manuscript received May 20, 2011; revised manuscript July 25, 2011
0002-9610/$ - see front matter © 2012 Elsevier Inc. All rights reserved. doi:10.1016/j.amjsurg.2011.07.015
dren. In 1999, Lew et al6 reported the largest cohort of pediatric BCVIs to date, on the basis of the National Pediatric Trauma Registry; their review identified an incidence of blunt carotid injuries of .03% (15 of 57,659 patients with blunt trauma). The authors speculated that this low incidence could be related to either underdiagnosis of injuries or actual decreased incidence compared with adults; a decrease in incidence could be due to innate, protective physiologic differences, namely, the lack of atherosclerotic disease and increased vascular elasticity in children. With few pediatric cases of BCVIs, management is currently based on isolated case reports, and the identification of injuries is often after neurologic deficits are discovered. There are no screening recommendations for BCVIs in children. The most recent Eastern Association for the Surgery of Trauma consensus guidelines support standard adult
8
The American Journal of Surgery, Vol 204, No 1, July 2012
screening triggers in the pediatric population.2 We questioned whether this screening protocol is appropriate on the basis of current epidemiology. The purpose of this study was to describe the incidence, injury patterns, presentation, and stroke rates of pediatric patients sustaining BCVIs.
Results
Methods All pediatric patients (aged ⱕ 18 years) diagnosed with BCVIs at our regional level I trauma center and pediatric level I trauma center since 1996 were reviewed. Denver Health Medical Center is a state-certified and American College of Surgeons–verified level I regional trauma center and an integral teaching facility of the University of Colorado School of Medicine. The Children’s Hospital is a level I regional pediatric trauma center and teaching facility of the University of Colorado. During the 1st portion of the study period, our screening test for patients at risk for BCVIs was 4-vessel cerebrovascular angiography; since 2007, multislice computed tomographic angiography (CTA) has become the preferred imaging modality as confidence in this test has been established.3–12 In patients who are candidates for antithrombotic therapy, screening is performed as soon as possible after evaluation of life-threatening injuries. Patients’ injuries were classified according to the Denver grading scale (Table 1).13 Once a BCVI was identified, either a carotid artery injury or a vertebral artery injury, antithrombotic therapy was started unless contraindicated by an associated injury at risk for bleeding. Initially, standard heparinization protocols were used, but because of a moderate incidence of bleeding in patients with multisystem trauma, the protocol was modified.14 The current anticoagulation protocol involves initiating systemic heparin as a continuous infusion of 15 U/kg/h, without a loading dose. The dosage was adjusted thereafter to achieve a partial thromboplastin time of 40 to 50 seconds. Alternatively, antiplatelet agents (aspirin 325 mg/d and/or clopidogrel 75 mg/d) were administered at the discretion of the attending surgeon. Statistical analysis was performed using SAS for Windows (SAS Institute Inc, Cary, NC). The Colorado Multi-Institutional Review Board approved this study.
Table 1
Denver grading scale for BCVI
Grade
Description
I
Irregularity of the vessel wall or a dissection or intramural hematoma with ⬍25% luminal stenosis Intraluminal thrombus or raised intimal flap is visualized, or dissection or intramural hematoma with ⱖ25% luminal narrowing Pseudoaneurysm Vessel occlusion Vessel transection
II
III IV V
From January 1996 to January 2010, 14,991 pediatric patients were admitted for blunt trauma, and 45 patients (.3%) were diagnosed with BCVIs. The majority (60%) were male, with a mean age of 13 ⫾ .7 years (range, 1.5–18 years) and a mean Injury Severity Score of 23 ⫾ 2. Thirtyone patients had carotid injuries, 11 had vertebral injuries, and 3 had both. Carotid injuries included 12 grade I injuries, 9 grade II injuries, 9 grade III injuries, 8 grade IV injuries, and 7 grade V injuries. Vertebral injuries included 6 grade I injuries, 2 grade II injuries, no grade III injuries, 8 grade IV injuries, 1 grade V injury. Mechanisms of injury included motor vehicle collisions (n ⫽ 24), automobile-pedestrian accidents (n ⫽ 9), direct blows to the neck (n ⫽ 2), falls (n ⫽ 2), motorcycle or snowmobile collisions (n ⫽ 2), assaults (n ⫽ 2), a snowboard accident (n ⫽ 1), a hanging (n ⫽ 1), and other mechanisms (n ⫽ 2). Associated injuries included cervical spine injuries (n ⫽ 19 [40%]), traumatic brain injuries (n ⫽ 16 [34%]), midface or mandible fractures (n ⫽ 9 [19%]), thoracic injuries (n ⫽ 16 [34%]), abdominal injuries (n ⫽ 14 [30%]), pelvic fractures (n ⫽ 11 [23%]), and extremity fractures (n ⫽ 15 [32%]). Mean intensive care unit and hospital lengths of stay were 14 ⫾ 1 and 18 ⫾ 1 days, respectively. Overall mortality was 9%. Thirty-two asymptomatic patients were diagnosed with BCVIs; 23 of these 32 patients (72%) met screening criteria according to adult protocols. Screening indications included cervical spine fractures (13 patients), skull fractures involving the carotid canal (3 patients), traumatic brain injuries or diffuse axonal injuries (3 patients), LeForte II or III fractures (3 patients), and mechanism of injury (1 patient). All but 1 of the asymptomatic patients were treated with antithrombotic agents, and 97% had no neurologic complications. One patient, who was a Jehovah’s Witness, with a grade IV injury (occlusion) of her right carotid artery and a grade II/III injury (⬎25% luminal narrowing/pseudoaneurysm) of her left carotid initially had a transient ischemic attack; for the first 48 hours, she was subtherapeutic on a heparin drip, but by hospital day 3, she was therapeutic. She developed neurologic symptoms with altered mental status and agitation early on day 4 and progressed to hemiplegia despite heparinization. Progressive luminal narrowing with high-grade stenosis was demonstrated on repeat CTA during the evaluation of the patient’s neurologic change, and she underwent carotid stenting of the left carotid artery. Three patients exsanguinated from carotid artery injuries. Ten patients (22%) presented with signs or symptoms of neurologic ischemia before diagnosis, with neurologic changes occurring a mean of 17 ⫾ 6 hours after injury (range, 1–72 hours); 91% of patients with stroke had carotid injuries as the etiology. Current adult BCVI screening indications for those patients with stroke were present in just 3 of the 10 patients (1 with marked soft tissue swelling, C-1 fracture, C-2 fracture). Of these 3 patients, 1 did not present with neurologic symptoms and did undergo screening CTA with a diagnosed grade I carotid injury; the patient could not
T.S. Jones et al.
Blunt cerebrovascular injuries in the child
be anticoagulated because of the traumatic brain injury and subsequently sustained a stroke approximately 72 hours after the injury. Five patients had major injuries that included skull fractures not involving the carotid canal (3 patients), mandible fracture (1 patient), and traumatic brain injury (1 patient). Two patients had no other identified injuries. Comparing asymptomatic patients with those with stroke, there was a significant difference in age (asymptomatic 15 ⫾ .5 years vs stroke 11 ⫾ 1.8 years). Twelve patients (27%) with BCVIs were ⱕ12 years old, and only 5 of these were asymptomatic at diagnosis. Thirty-one patients were diagnosed via arteriography, and 12 patients were diagnosed with CTA. Two patients who exsanguinated were diagnosed before imaging was completed. Mean creatinine at the time of admission was .7 mg/dL, and after 48 hours, mean creatinine was .6 mg/dL. One patient sustained acute kidney injury after posttraumatic nephrectomy. No patient required dialysis during hospitalization. One patient, who had bilateral occlusion of her vertebral arteries, developed gastrointestinal bleeding on hospital day 12, 1 week after the initiation of a heparin drip. She was noted to have gastric ulcerations in her stomach during endoscopy for percutaneous gastrostomy tube placement on hospital day 5. Her heparin drip was discontinued, and she required a total of 3 U of packed red blood cells. She was started on low–molecular weight heparin for prophylaxis and did not develop any neurologic symptoms.
Comments BCVIs are believed to be a rare phenomenon in the pediatric population. The most recent Eastern Association for the Surgery of Trauma consensus guidelines support standard adult screening triggers for children.2 Upon review of the current literature, however, there is a paucity of data to suggest these are appropriate guidelines for the pediatric age range. In our evaluation, 45 children were found to have BCVIs, with an incidence of .3% of all blunt pediatric trauma admissions. This incidence is significantly higher than previous retrospective reviews for pediatric populations,6 likely because of an increased awareness and aggressive screening at our institution. Only 72% of asymptomatic pediatric patients with BCVIs had screening criteria according to adult protocols, and of those presenting with neurologic findings, more than two thirds did not have screening indications. Screening criteria that could be modified for children include injury pattern and mechanism. In addition to the adult screening criteria, the incidence of nonbasilar skull fracture and chest trauma was particularly high among symptomatic patients. Among asymptomatic patients, nonbasilar skull fracture, chest trauma, and traumatic brain injury were the most common. Previous studies have demonstrated a 4-fold to 8-fold risk for BCVI in children and adults with any chest trauma; isolated clavicle fractures are
9 associated with an 8-fold increase in BCVI risk.6,15 In addition to high-velocity mechanisms such as motor vehicle collisions and automobile-pedestrian accidents, low-impact trauma including short-distance falls and direct blows were also implicated in several patients with carotid injuries in our population. As indicated in previous case reports, these mechanisms, however benign sounding, can result in BCVIs, often with significant neurologic deficits before presentation.16 –18 For all age groups, it is important to include mechanism as a screening trigger in addition to clinical presentation. All of our patients were involved in either high-mechanism trauma (motor vehicle collisions, automobile-pedestrian accidents, motorcycle collisions, falls, and snowboarding collisions in 84%), or they sustained direct trauma to the neck (assault and hanging in 16%). There is a proven reduction in stroke rate for both carotid and vertebral artery injuries with antithrombotic treatment.19,20 Therefore, screening during the asymptomatic period before the onset of stroke is critical. CTA has been shown to be sensitive and specific for neck and extremity pediatric trauma,21 but there are concerns that increased screening would result in an increased radiation risk for more children, and that magnetic resonance angiography (MRA) is a better choice for children. Several studies comparing CTA with MRA for BCVI have shown lower sensitivity and specificity for MRA (50%–75% and 47%– 67%, respectively),22 so MRA has not been advocated as an optimal screening modality, but there have been no recent reports comparing the efficacy of MRA with that of CTA. There was a documented latent period in these patients, which could afford time for diagnosis and treatment. Of the initially asymptomatic patients with diagnosed BCVI, 1 patient had neurologic changes after heparinization and was subsequently treated with carotid stenting. With only 1 complication related to antithrombotic therapy, treatment to prevent stroke appears safe. There were several limitations of this study. This was a retrospective review of our data, not a randomized controlled trial. Many patients were not compliant with follow-up imaging, so the long-term histories of these injuries are unknown. Finally, the type of antithrombotic treatment (heparin vs antiplatelet agents) was individualized at the surgeon’s discretion. Before the development of screening guidelines, there was a BCVI rate of .08% to .17% in all blunt trauma admissions.14 After implementation of the screening protocols, 39% to 41% of patients who had 1 of the screening factors had identified BCVIs.23 Once thought to be a rare occurrence, BCVIs are now diagnosed in ⬎1% of adult patients with blunt trauma. The incidence of BCVIs in children is significantly higher than previously suspected, and historically patients have presented after neurologic deterioration. With effective stroke prevention in children with antithrombotic agents, early screening for BCVIs and associated treatment should be pursued. With the increased availability and ease of noninvasive imaging with CTA, in
10
The American Journal of Surgery, Vol 204, No 1, July 2012
addition to the devastating morbidity associated with missed injuries, broader screening guidelines for children should be instituted.
11. Utter GH, Hollingworth W, Hallam DK, et al. Sixteen-slice CT angiography in patients with suspected blunt carotid and vertebral artery injuries. J Am Coll Surg 2006;203:838 – 48. 12. Biffl WL, Egglin T, Benedetto B, et al. Sixteen-slice computed tomographic angiography is a reliable noninvasive screening test for clinically significant blunt cerebrovascular injuries. J Trauma 2006;60: 745–51. 13. Biffl WL, Moore EE, Offner PJ, et al. Blunt carotid arterial injuries: implications of a new grading scale. J Trauma 1999;47:845–53. 14. Biffl WL, Moore EE, Ryu RK, et al. The unrecognized epidemic of blunt carotid arterial injuries: early diagnosis improves neurologic outcome. Ann Surg 1998;228:462–70. 15. Parikh AA, Luchette FA, Valente JF, et al. Blunt carotid artery injuries. J Am Coll Surg 1997;185:80 – 6. 16. Cuff RF, Thomas JH. Pediatric blunt carotid injury from low impact trauma: a case report and review of the literature. J Trauma 2005;58: 620 –3. 17. Payton TF, Siddiqui KM, Sole DP, et al. Traumatic dissection of the internal carotid artery. Pediatr Emerg Care 2004;20:27–9. 18. Lin JJ, Chou ML, Lin KL, et al. Cerebral infarct secondary to traumatic carotid artery dissection. Pediatr Emerg Care 2007;23: 166 – 8. 19. Cothren CC, Biffl WL, Moore EE, et al. Treatment for blunt cerebrovascular injuries: Equivalence of anticoagulation and antiplatelet agents. Arch Surg 2009;44:685–90. 20. Miller PR, Fabian TC, Croce MA, et al. Prospective screening for blunt cerebrovascular injuries: analysis of diagnostic modalities and outcomes. Ann Surg 2002;236:386 –93. 21. Hohan AR, Lineen EB, Perez EA, et al. Value of computed tomographic angiography in neck and extremity pediatric vascular trauma. J Pediatr Surg 2009;44:1236 – 42. 22. Biffl WL. Diagnosis of blunt cerebrovascular injuries. Curr Opin Crit Care 2003;9:530 – 4. 23. Cothren CC, Moore EE, Ray CE, et al. Screening for blunt cerebrovascular injuries is cost effective. Am J Surg 2005;190:845–9.
References 1. Krajweski LP, Hertzer NR. Blunt carotid artery trauma: report of two cases and review of the literature. Ann Surg 1980;191:341– 6. 2. Bromberg WJ, Collier BC, Diebel LN, et al. Blunt cerebrovascular injury practice management guidelines: the Eastern Association for the Surgery of Trauma. J Trauma 2010;68:471–7. 3. Biffl WL, Cothren CC, Moore EE, et al. Western Trauma Association critical decisions in trauma: screening for and treatment of blunt cerebrovascular injuries. J Trauma 2009;67:1150 –3. 4. Burlew CC, Biffl WL. Blunt cerebrovascular trauma. Curr Opin Crit Care 2010;16:587–95. 5. Burlew CC, Biffl WL. Imaging for blunt carotid and vertebral artery injuries. Surg Clin North Am 2011;91:217–31. 6. Lew SM, Frumiento C, Wald SL. Pediatric blunt carotid injury: a review of the National Pediatric Trauma Registry. Pediatr Neurosurg 1999;l30:239 – 44. 7. Berne JD, Reuland KS, Villarreal DH, et al. Sixteen-slice multidetector computed tomographic angiography improves the accuracy of screening for blunt cerebrovascular injury. J Trauma 2006;60:1204 –9. 8. Bub LD, Hollingworth W, Jarvik JG, et al. Screening for blunt cerebrovascular injury: Evaluating the accuracy of multidetector computed tomographic angiography. J Trauma 2005;59:691–7. 9. Schneidereit NP, Simons R, Nicolau S, et al. Utility of screening for blunt vascular neck injuries with computed tomographic angiography. J Trauma 2006;60:209 –16. 10. Eastman AL, Chason DP, Perez CL, et al. Computed tomographic angiography for the diagnosis of blunt cervical vascular injury: is it ready for primetime? J Trauma 2006;60:925–9.