http://informahealthcare.com/bij ISSN: 0269-9052 (print), 1362-301X (electronic) Brain Inj, 2014; 28(12): 1617–1621 ! 2014 Informa UK Ltd. DOI: 10.3109/02699052.2014.934284
CASE STUDY
Impalement brain injury from steel rod causing injury to jugular bulb: Case report and review of the literature Andrew J. Grossbach1, Taylor J. Abel1, Janel Smietana1, Nader Dahdaleh2, Meryl A. Severson III3 & David Hasan1 1
Department of Neurosurgery, University of Iowa Hospitals and Clinics, Iowa City, IA, USA, 2Department of Neurosurgery, Northwestern University, Chicago, IL, USA, and 3Division of Neurosurgery, National Capitol Consortium, Walter Reed National Military Medical Center, Bethesda, MD, USA
Abstract
Keywords
Background: The management of impalement penetrating brain injuries (IPBI) from non-missile objects is extremely challenging, especially when vascular structures are involved. Cerebral angiography is a crucial tool in initial evaluation to assess for vascular injury as standard non-invasive imaging modalities are limited by foreign body artifact, especially for metallic objects. Case study: This study reports a case of an IPBI caused by a segment of steel rebar resulting in injury to the left jugular bulb and posterior temporal lobe. It describes the initial presentation, radiology, management and outcome in this patient and reviews the literature of similar injuries.
Angiogram, rebar, traumatic brain injury, vascular
Introduction Penetrating brain injuries (PBIs) are a type of traumatic brain injury that can be separated into two categories, missile and non-missile injuries [1]. Missile injuries result from an object penetrating the brain travelling at 4100 m s 1 and results in brain injury from both kinetic and thermal energy [1, 2]. Non-missile PBIs are relatively uncommon injuries in the US that result from various causes including motor vehicle accidents, falls, violence, self-inflicted trauma and work accidents [3, 4]. Although these injuries are often fatal [5], patients who do survive the initial injury pose a unique set of problems that must be addressed during management [3, 4]. There have been several reports of non-missile PBIs in the literature resulting from impalement by various objects, most commonly metallic objects [1, 3, 4, 6, 7]. This manuscript describes the presentation and management of a patient who was impaled by a segment of steel bar and reviews the management of impalement penetrating brain injuries.
Case report History and physical A 22-year-old male presented to the University of Iowa Hospitals and Clinics after a 12 foot fall from a ladder while working at a construction site. The patient landed upright on a piece of steel reinforcing bar (rebar) that penetrated his neck and extended intracranially. Emergency services Correspondence: Andrew J. Grossbach, MD, Department of Neurosurgery, University of Iowa Hospitals and Clinics, 200 Hawkins Drive, Iowa City, IA, 52245, USA. Tel: 206-679-2197. E-mail: [email protected]
History Received 6 November 2013 Revised 28 January 2014 Accepted 6 June 2014 Published online 14 July 2014
responded at the scene and cut the rebar from the concrete from which it was imbedded. The patient was taken to the emergency department with the rebar in place. He was intubated en route after becoming combative. Upon arrival in the emergency department, the patient was noted to be stuporous. His pupils were equal and reactive. The patient was moving all extremities spontaneously, but not following commands. The rebar was noted to be piercing the left neck and extending cranially (Figure 1). A non-contrast computed tomography (CT) scan of the head was obtained that showed the rebar had punctured the soft tissues of the neck, travelled posterior to the mandible and penetrated the skull base, traversing the medial mastoid air cells and jugular fossa on the left (Figures 1 and 2). The bar also pierced the left posterior temporal lobe with termination in the left temporoparietal region. There was intraparenchymal haemorrhage along the tract of the rebar, ventricular haemorrhage in the left lateral ventricle and a left subdural haemorrhage causing midline shift (Figure 1). A CT angiogram (CTA) of the head and neck was performed and did not show any evidence of injury to the intracranial arteries; however, the scan was severely limited by metallic artifact. Operation The patient was taken emergently to the operating room where a right-sided ventriculostomy was placed for ICP monitoring and drainage of cerebrospinal fluid (CSF). Given the injury to the soft tissues of the neck and concern for swelling, a tracheostomy was performed. An emergent diagnostic cerebral angiogram was performed prior to craniotomy, given the high concern for injury to the cerebral
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Figure 1. (A) Pre-operative photograph demonstrating entry site and trajectory of rebar. (B) Lateral XR showing the relationship of the rebar to the cranium. There was haemorrhage along the tract of the rebar, intraventricular haemorrhage and a subdural haematoma evident on non-contrast CT (C). The position of the rebar is depicted on coronal (D), sagittal (E) and axial (F) CT scans.
Figure 2. 3-D CT reconstruction demonstrating the entry point of the rebar in relation to the cranial bones.
vasculature due to the trajectory of the rebar despite the negative CTA. The angiogram showed no injury to the intracranial or cervical arteries (Figure 3), however, extravasation of the contrast dye was seen from the left jugular bulb (Figure 4A). A SynchroSoft microwire and SL10 microcatheter were used to perform a coil embolization of the left sigmoid sinus along with coil embolization and onyx embolization of the left jugular bulb (Figure 4B). The patient was then repositioned and underwent a left hemicraniectomy. A mastoidectomy was performed to expose the transverse sinus, sigmoid sinus and cervical internal jugular vein, which was ligated. The dura was then opened to remove the SDH. Once proximal control of the sigmoid sinus was obtained and the jugular bulb visualized, the segment of rebar was carefully removed. The rebar could be seen disrupting
the jugular bulb. There was minimal haemorrhage after rebar removal and hemostasis was achieved using standard techniques. A second diagnostic cerebral angiogram was performed to confirm that there was no dissection and satisfactory occlusion of the left sigmoid sinus and jugular bulb (Figure 4). Post-operative course Post-operatively, the patient was admitted to the ICU for monitoring. The ventriculostomy was slowly weaned and was removed on post-operative day 11. The patient was initially comatose; however, made a steady recovery. He initially exhibited a Wernicke’s aphasia; however, by discharge on post-operative day 15 to a rehabilitation facility, the patient
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DOI: 10.3109/02699052.2014.934284
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Figure 3. Cerebral angiogram demonstrating position of rebar (arrows in (A) and (B)) in relation to the cerebral vasculature. (A) AP left internal carotid artery injection and (B) lateral left internal carotid artery injection.
Figure 4. Cerebral angiogram demonstrating extravasation of contrast dye from left jugular bulb during angiogram (vertical arrow, horizontal arrows depict rebar). (D) Coil and onyx embolization of the left sigmoid sinus and jugular bulb (arrows).
was able to follow simple commands, speak a few short sentences and was oriented to self. He was ambulatory, although he had a mild right-sided hemiparesis. He also had a dense right hemianopia. Upon follow-up 6 weeks after injury, the patient was oriented to person and place. His aphasia had resolved and he was full strength in all four extremities. His right hemianopia persisted. It was noted that he had some build-up of fluid under his cranial incision and a head CT revealed a CSF fluid collection. The patient underwent placement of a ventriculo-peritoneal shunt and a left-sided native bone cranioplasty without complication. One year after injury, the patient underwent formal neuropsychological evaluation that demonstrated deficits in attention, complex organization, verbal memory and processing speed. On the most recent follow-up, 18 months postinjury, the patient exhibited significant improvement in many of his baseline functions, with the exception of his dense right hemianopia and seemingly mild cognitive slowing.
Discussion Impalement brain injuries pose unique challenges to surgeons [3, 6–8]. These injuries often involve the orbit or temporal areas, as these areas have thinner calvarium that is more susceptible to penetration [1]. Several factors need to be taken into account including associated trauma, the characteristics of the penetrating object, the location of the penetration and structures that could be involved, as well as the possibility of vascular injury [4]. When dealing with PBIs, as with any traumatic brain injury, secondary injury can be common from mechanisms including increased ICP, hypotension, respiratory distress and coagulopathy, all of which have been associated with increased mortality in PBI patients [3, 5]. Additionally, PBI management can be complicated by infection, cerebrospinal fluid leak and cerebral vasospasm [9]. Pre-hospital care should focus on standard Advanced Trauma Life Support (ATLS) principles, the ‘ABCs’,
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including airway, breathing and cardiovascular support [10]. The penetrating object should not be removed in the field if it can be avoided. Cutting the penetrating object can be considered to make the object and patient more mobile. Care should be taken to disturb the object as little as possible during transport. Initial pre-operative imaging should be performed with a non-contrast computed tomography (CT) scan [7]. This is especially true when dealing with a metallic object. Magnetic resonance imaging (MRI) may be useful to identify penetrating objects made of wood [1, 7]; however, it is contraindicated when dealing with potentially ferromagnetic objects. Pre-operative cerebral angiography should be performed if there is any concern for intracranial vascular injury [4, 6, 7, 9, 11]. In their series on intracranial stab wounds, Kieck and de Villiers [6] report intracranial vascular injury in 20% of their total patients and 33% of the patients who underwent angiography [6]. Intracranial vascular injuries can range from carotid-cavernous and other arteriovenous fistulas, aneurysms, pseudoaneurysms, arterial transections or occlusions and vasospasm [9, 12, 13]. The use of CTangiography (CTA) or MR-angiography (MRA) has been increasing; however, conventional cerebral angiography remains the gold standard [4, 14]. CTA and MRA may exhibit artifact, making accurate interpretation difficult or impossible [4]. This study recommends digital subtraction angiography in all cases of penetrating brain injury, as the possibility of cerebrovascular injury exists by the very nature of the injury. Delayed follow-up angiography is also recommended as pseudoaneurysms can frequently present in a delayed fashion [6, 9, 15–17]. Early post-operative CT is important to identify possible intracranial haemorrhage obscured by artifacts from the foreign body during initial scanning [11]. Removal of the offending object should be done under direct visualization in a controlled manner in the operating room using a craniotomy due to risk of potentially fatal haemorrhage [1, 4, 7, 8]. Angiography should be used to evaluate for vascular injury and vascular control should be obtained prior to removal via endovascular techniques [15]; however, some authors recommend craniotomy for direct hemostasis of vascular injuries due to possible delay in obtaining angiography [11]. When removing embedded penetrating foreign objects the standard goals of surgery in these institutions are removal under direct vision with proximal and distal vascular control; cerebral decompression; evacuation of mass lesions (EDH, SDH, IPH); debridement of necrotic tissue; hemostasis; and CSF diversion for ICP monitoring and to reduce the risk of CSF leak [9, 18]. While the literature is lacking with regard to ICP monitoring in PBI patients, this practice is the standard in accordance with the head injury management guidelines [8, 9, 11, 18]. Dural closure should be attempted if a craniectomy is not performed to reduce the risk of post-operative cerebral spinal fluid (CSF) leak [11]. The use of ICP monitoring is relatively uncommon in PBI patients, likely due to high initial mortality and lack of reporting in the literature, but elevated ICPs have been associated with increased mortality [5]. The use of antibiotics in the context of PBI is controversial in terms of antibiotic selection and time course of therapy,
Brain Inj, 2014; 28(12): 1617–1621
however, it is generally recommended that broad-spectrum antibiotics with good CNS penetration be used for 7–14 days [9], as meningitis and cerebral abscesses may be complications resulting from low-velocity penetrating brain injuries [1, 4, 11, 14]. Currently, there are no evidence-based guidelines to dictate duration of antibiotic use. Potential contamination from the penetrating object must be taken into account on a case-by-case basis. Post-traumatic epilepsy (PTE) is also a common complication of PBI [8, 19]. PTE after penetrating brain injury is more common than in blunt TBI and is reported in up to 50% of patients and can occur decades after injury [20, 21]. Prophylactic anti-epileptic medications are frequently used, although none has been demonstrated to prevent posttraumatic epilepsy and recommended duration of therapy varies significantly [2, 8, 12, 14]. The Brain Trauma Foundation Guidelines offer a Level II recommendation that prophylactic use of phenytoin or valproate are not recommended to prevent late post-traumatic seizures while anticonvulsant use is indicated to prevent early seizures within 7 days of injury [22]. In practice, the authors typically employ either phenytoin or levetiracetam for 7 days post-injury. When dealing with PBIs, low initial Glasgow Coma Scale (GCS) and advanced age are associated with poor outcomes [3, 5]. Suicide as a mechanism of injury is also correlated with a higher mortality [5]. Despite the high mortality rate for penetrating brain injuries, this case illustrates that, if properly managed, these patients have the ability to significantly recover from their severe injuries. Further study is needed to determine appropriate PBI seizure prophylaxis as well as antibiotic therapy.
Declaration of interest The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References 1. Schreckinger M, Orringer D, Thompson BG, La Marca F, Sagher O. Transorbital penetrating injury: Case series, review of the literature, and proposed management algorithm. Journal of Neurosurgery 2011;114:53–61. 2. Kothari K, Singh AK, Das S. Penetrating skull injury with six inch fence rod. National Journal of Maxillofacical Surgery 2012;3: 207–210. 3. Syrmos N, Ganau M, De Carlo A, Prisco L, Ganau L, Valadakis V, Grigoriou K, Iliadis C, Arvanitakis D. Dealing with the surgical and medical challenges of penetrating brain injuries. Case Reports in Surgery 2013. 4. Selvanathan S, Goldschlager T, McMillen J, Campbell S. Penetrating craniocerebral injuries from nail-gun use. Journal of Clinical Neuroscience 2007;14:678–683. 5. Aarabi B, Alden TD, Chestnut RM, et al. Management and prognosis of penetrating brain injury—guidelines. J Trauma 2001; 51(Suppl):S1–86. 6. Kieck CF, de Villiers JC. Vascular-lesions due to transcranial stab wounds. Journal of Neurosurgery 1984;60:42–46. 7. Azarpira N, Pourjafar M, Neghad MN. Penetrating knife injury to the temporal lobe: A case report. Neurosurgery Quarterly 2013;23: 64–65. 8. Karim T, Topno M. An unusual case of penetrating head injury in a child. Journal of Emergencies, Trauma & Shock 2010;3:197–198. 9. Kazim SF, Shamim MS, Tahir MZ, Enam SA, Waheed S. Management of penetrating brain injury. Journal of Emergencies, Trauma & Shock 2011;4:395–402.
DOI: 10.3109/02699052.2014.934284
10. Nicolaisen N, Ahmed A, Hancock T, Ogren R. Field airway management of a construction worker with an impaling rebar injury to the neck and brain. Prehospital Emergency Care: Official Journal of the National Association of EMS Physicians and the National Association of State EMS Directors. 2012;16:548–552. 11. Lin HL, Lee HC, Cho DY. Management of transorbital brain injury. Journal of the Chinese Medical Association 2007;70:36–38. 12. Pascual JM, Navas M, Carrasco R. Penetrating ballistic-like frontal brain injury caused by a metallic rod. Acta Neurochirurgica (Wien) 2009;151:689–691. 13. Bell RS, Vo AH, Roberts R, Wanebo J, Armonda RA. Wartime traumatic aneurysms: Acute presentation, diagnosis, and multimodal treatment of 64 craniocervical arterial injuries. Neurosurgery 2010;66:66–79; discussion. 14. Sonmez E, Borcek AO, Guven C, Hasturk AE. An iron rod stuck in the right motor cortex. Turkish Neurosurgery 2012;22: 772–774. 15. du Trevou MD, van Dellen JR. Penetrating stab wounds to the brain: The timing of angiography in patients presenting with the weapon already removed. Neurosurgery 1992;31:905–911; discussion 11–12. 16. Al-Mefty O, Holoubi A, Fox JL. Value of angiography in cerebral nail-gun injuries. American Journal of Neuroradiology 1986;7: 164–165.
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17. Litvack ZN, Hunt MA, Weinstein JS, West GA. Self-inflicted nail-gun injury with 12 cranial penetrations and associated cerebral trauma. Case report and review of the literature. Journal of Neurosurgery 2006;104:828–834. 18. Bratton SL, Chestnut RM, Ghajar J, McConnell Hammond FF, Harris OA, Hartl R, Manley GT, Nemecek A, Newell DW, Rosenthal G, et al. Guidelines for the management of severe traumatic brain injury. VI. Indications for intracranial pressure monitoring. Journal of Neurotrauma 2007;24(Suppl 1):S37–S44. 19. Salazar AM, Schwab K, Grafman JH. Penetrating injuries in the Vietnam war. Traumatic unconsciousness, epilepsy, and psychosocial outcome. Neurosurgery Clinics of North America 1995;6: 715–726. 20. Raymont V, Salazar AM, Lipsky R, Goldman D, Tasick G, Grafman J. Correlates of posttraumatic epilepsy 35 years following combat brain injury. Neurology 2010;75:224–229. 21. Chen JW, Ruff RL, Eavey R, Wasterlain CG. Posttraumatic epilepsy and treatment. Journal of Rehabilitation Research and Development 2009;46:685–696. 22. Bratton SL, Chestnut RM, Ghajar J, McConnell Hammond FF, Harris OA, Hartl R, Manley GT, Nemecek A, Newell DW, Rosenthal G, et al. Guidelines for the management of severe traumatic brain injury. XIII. Antiseizure prophylaxis. Journal of Neurotrauma 2006;24(Suppl 1):S83–S86.
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CASE STUDY
Impalement brain injury from steel rod causing injury to jugular bulb: Case report and review of the literature Andrew J. Grossbach1, Taylor J. Abel1, Janel Smietana1, Nader Dahdaleh2, Meryl A. Severson III3 & David Hasan1 1
Department of Neurosurgery, University of Iowa Hospitals and Clinics, Iowa City, IA, USA, 2Department of Neurosurgery, Northwestern University, Chicago, IL, USA, and 3Division of Neurosurgery, National Capitol Consortium, Walter Reed National Military Medical Center, Bethesda, MD, USA
Abstract
Keywords
Background: The management of impalement penetrating brain injuries (IPBI) from non-missile objects is extremely challenging, especially when vascular structures are involved. Cerebral angiography is a crucial tool in initial evaluation to assess for vascular injury as standard non-invasive imaging modalities are limited by foreign body artifact, especially for metallic objects. Case study: This study reports a case of an IPBI caused by a segment of steel rebar resulting in injury to the left jugular bulb and posterior temporal lobe. It describes the initial presentation, radiology, management and outcome in this patient and reviews the literature of similar injuries.
Angiogram, rebar, traumatic brain injury, vascular
Introduction Penetrating brain injuries (PBIs) are a type of traumatic brain injury that can be separated into two categories, missile and non-missile injuries [1]. Missile injuries result from an object penetrating the brain travelling at 4100 m s 1 and results in brain injury from both kinetic and thermal energy [1, 2]. Non-missile PBIs are relatively uncommon injuries in the US that result from various causes including motor vehicle accidents, falls, violence, self-inflicted trauma and work accidents [3, 4]. Although these injuries are often fatal [5], patients who do survive the initial injury pose a unique set of problems that must be addressed during management [3, 4]. There have been several reports of non-missile PBIs in the literature resulting from impalement by various objects, most commonly metallic objects [1, 3, 4, 6, 7]. This manuscript describes the presentation and management of a patient who was impaled by a segment of steel bar and reviews the management of impalement penetrating brain injuries.
Case report History and physical A 22-year-old male presented to the University of Iowa Hospitals and Clinics after a 12 foot fall from a ladder while working at a construction site. The patient landed upright on a piece of steel reinforcing bar (rebar) that penetrated his neck and extended intracranially. Emergency services Correspondence: Andrew J. Grossbach, MD, Department of Neurosurgery, University of Iowa Hospitals and Clinics, 200 Hawkins Drive, Iowa City, IA, 52245, USA. Tel: 206-679-2197. E-mail: [email protected]
History Received 6 November 2013 Revised 28 January 2014 Accepted 6 June 2014 Published online 14 July 2014
responded at the scene and cut the rebar from the concrete from which it was imbedded. The patient was taken to the emergency department with the rebar in place. He was intubated en route after becoming combative. Upon arrival in the emergency department, the patient was noted to be stuporous. His pupils were equal and reactive. The patient was moving all extremities spontaneously, but not following commands. The rebar was noted to be piercing the left neck and extending cranially (Figure 1). A non-contrast computed tomography (CT) scan of the head was obtained that showed the rebar had punctured the soft tissues of the neck, travelled posterior to the mandible and penetrated the skull base, traversing the medial mastoid air cells and jugular fossa on the left (Figures 1 and 2). The bar also pierced the left posterior temporal lobe with termination in the left temporoparietal region. There was intraparenchymal haemorrhage along the tract of the rebar, ventricular haemorrhage in the left lateral ventricle and a left subdural haemorrhage causing midline shift (Figure 1). A CT angiogram (CTA) of the head and neck was performed and did not show any evidence of injury to the intracranial arteries; however, the scan was severely limited by metallic artifact. Operation The patient was taken emergently to the operating room where a right-sided ventriculostomy was placed for ICP monitoring and drainage of cerebrospinal fluid (CSF). Given the injury to the soft tissues of the neck and concern for swelling, a tracheostomy was performed. An emergent diagnostic cerebral angiogram was performed prior to craniotomy, given the high concern for injury to the cerebral
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Brain Inj, 2014; 28(12): 1617–1621
Figure 1. (A) Pre-operative photograph demonstrating entry site and trajectory of rebar. (B) Lateral XR showing the relationship of the rebar to the cranium. There was haemorrhage along the tract of the rebar, intraventricular haemorrhage and a subdural haematoma evident on non-contrast CT (C). The position of the rebar is depicted on coronal (D), sagittal (E) and axial (F) CT scans.
Figure 2. 3-D CT reconstruction demonstrating the entry point of the rebar in relation to the cranial bones.
vasculature due to the trajectory of the rebar despite the negative CTA. The angiogram showed no injury to the intracranial or cervical arteries (Figure 3), however, extravasation of the contrast dye was seen from the left jugular bulb (Figure 4A). A SynchroSoft microwire and SL10 microcatheter were used to perform a coil embolization of the left sigmoid sinus along with coil embolization and onyx embolization of the left jugular bulb (Figure 4B). The patient was then repositioned and underwent a left hemicraniectomy. A mastoidectomy was performed to expose the transverse sinus, sigmoid sinus and cervical internal jugular vein, which was ligated. The dura was then opened to remove the SDH. Once proximal control of the sigmoid sinus was obtained and the jugular bulb visualized, the segment of rebar was carefully removed. The rebar could be seen disrupting
the jugular bulb. There was minimal haemorrhage after rebar removal and hemostasis was achieved using standard techniques. A second diagnostic cerebral angiogram was performed to confirm that there was no dissection and satisfactory occlusion of the left sigmoid sinus and jugular bulb (Figure 4). Post-operative course Post-operatively, the patient was admitted to the ICU for monitoring. The ventriculostomy was slowly weaned and was removed on post-operative day 11. The patient was initially comatose; however, made a steady recovery. He initially exhibited a Wernicke’s aphasia; however, by discharge on post-operative day 15 to a rehabilitation facility, the patient
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DOI: 10.3109/02699052.2014.934284
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Figure 3. Cerebral angiogram demonstrating position of rebar (arrows in (A) and (B)) in relation to the cerebral vasculature. (A) AP left internal carotid artery injection and (B) lateral left internal carotid artery injection.
Figure 4. Cerebral angiogram demonstrating extravasation of contrast dye from left jugular bulb during angiogram (vertical arrow, horizontal arrows depict rebar). (D) Coil and onyx embolization of the left sigmoid sinus and jugular bulb (arrows).
was able to follow simple commands, speak a few short sentences and was oriented to self. He was ambulatory, although he had a mild right-sided hemiparesis. He also had a dense right hemianopia. Upon follow-up 6 weeks after injury, the patient was oriented to person and place. His aphasia had resolved and he was full strength in all four extremities. His right hemianopia persisted. It was noted that he had some build-up of fluid under his cranial incision and a head CT revealed a CSF fluid collection. The patient underwent placement of a ventriculo-peritoneal shunt and a left-sided native bone cranioplasty without complication. One year after injury, the patient underwent formal neuropsychological evaluation that demonstrated deficits in attention, complex organization, verbal memory and processing speed. On the most recent follow-up, 18 months postinjury, the patient exhibited significant improvement in many of his baseline functions, with the exception of his dense right hemianopia and seemingly mild cognitive slowing.
Discussion Impalement brain injuries pose unique challenges to surgeons [3, 6–8]. These injuries often involve the orbit or temporal areas, as these areas have thinner calvarium that is more susceptible to penetration [1]. Several factors need to be taken into account including associated trauma, the characteristics of the penetrating object, the location of the penetration and structures that could be involved, as well as the possibility of vascular injury [4]. When dealing with PBIs, as with any traumatic brain injury, secondary injury can be common from mechanisms including increased ICP, hypotension, respiratory distress and coagulopathy, all of which have been associated with increased mortality in PBI patients [3, 5]. Additionally, PBI management can be complicated by infection, cerebrospinal fluid leak and cerebral vasospasm [9]. Pre-hospital care should focus on standard Advanced Trauma Life Support (ATLS) principles, the ‘ABCs’,
1620
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including airway, breathing and cardiovascular support [10]. The penetrating object should not be removed in the field if it can be avoided. Cutting the penetrating object can be considered to make the object and patient more mobile. Care should be taken to disturb the object as little as possible during transport. Initial pre-operative imaging should be performed with a non-contrast computed tomography (CT) scan [7]. This is especially true when dealing with a metallic object. Magnetic resonance imaging (MRI) may be useful to identify penetrating objects made of wood [1, 7]; however, it is contraindicated when dealing with potentially ferromagnetic objects. Pre-operative cerebral angiography should be performed if there is any concern for intracranial vascular injury [4, 6, 7, 9, 11]. In their series on intracranial stab wounds, Kieck and de Villiers [6] report intracranial vascular injury in 20% of their total patients and 33% of the patients who underwent angiography [6]. Intracranial vascular injuries can range from carotid-cavernous and other arteriovenous fistulas, aneurysms, pseudoaneurysms, arterial transections or occlusions and vasospasm [9, 12, 13]. The use of CTangiography (CTA) or MR-angiography (MRA) has been increasing; however, conventional cerebral angiography remains the gold standard [4, 14]. CTA and MRA may exhibit artifact, making accurate interpretation difficult or impossible [4]. This study recommends digital subtraction angiography in all cases of penetrating brain injury, as the possibility of cerebrovascular injury exists by the very nature of the injury. Delayed follow-up angiography is also recommended as pseudoaneurysms can frequently present in a delayed fashion [6, 9, 15–17]. Early post-operative CT is important to identify possible intracranial haemorrhage obscured by artifacts from the foreign body during initial scanning [11]. Removal of the offending object should be done under direct visualization in a controlled manner in the operating room using a craniotomy due to risk of potentially fatal haemorrhage [1, 4, 7, 8]. Angiography should be used to evaluate for vascular injury and vascular control should be obtained prior to removal via endovascular techniques [15]; however, some authors recommend craniotomy for direct hemostasis of vascular injuries due to possible delay in obtaining angiography [11]. When removing embedded penetrating foreign objects the standard goals of surgery in these institutions are removal under direct vision with proximal and distal vascular control; cerebral decompression; evacuation of mass lesions (EDH, SDH, IPH); debridement of necrotic tissue; hemostasis; and CSF diversion for ICP monitoring and to reduce the risk of CSF leak [9, 18]. While the literature is lacking with regard to ICP monitoring in PBI patients, this practice is the standard in accordance with the head injury management guidelines [8, 9, 11, 18]. Dural closure should be attempted if a craniectomy is not performed to reduce the risk of post-operative cerebral spinal fluid (CSF) leak [11]. The use of ICP monitoring is relatively uncommon in PBI patients, likely due to high initial mortality and lack of reporting in the literature, but elevated ICPs have been associated with increased mortality [5]. The use of antibiotics in the context of PBI is controversial in terms of antibiotic selection and time course of therapy,
Brain Inj, 2014; 28(12): 1617–1621
however, it is generally recommended that broad-spectrum antibiotics with good CNS penetration be used for 7–14 days [9], as meningitis and cerebral abscesses may be complications resulting from low-velocity penetrating brain injuries [1, 4, 11, 14]. Currently, there are no evidence-based guidelines to dictate duration of antibiotic use. Potential contamination from the penetrating object must be taken into account on a case-by-case basis. Post-traumatic epilepsy (PTE) is also a common complication of PBI [8, 19]. PTE after penetrating brain injury is more common than in blunt TBI and is reported in up to 50% of patients and can occur decades after injury [20, 21]. Prophylactic anti-epileptic medications are frequently used, although none has been demonstrated to prevent posttraumatic epilepsy and recommended duration of therapy varies significantly [2, 8, 12, 14]. The Brain Trauma Foundation Guidelines offer a Level II recommendation that prophylactic use of phenytoin or valproate are not recommended to prevent late post-traumatic seizures while anticonvulsant use is indicated to prevent early seizures within 7 days of injury [22]. In practice, the authors typically employ either phenytoin or levetiracetam for 7 days post-injury. When dealing with PBIs, low initial Glasgow Coma Scale (GCS) and advanced age are associated with poor outcomes [3, 5]. Suicide as a mechanism of injury is also correlated with a higher mortality [5]. Despite the high mortality rate for penetrating brain injuries, this case illustrates that, if properly managed, these patients have the ability to significantly recover from their severe injuries. Further study is needed to determine appropriate PBI seizure prophylaxis as well as antibiotic therapy.
Declaration of interest The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References 1. Schreckinger M, Orringer D, Thompson BG, La Marca F, Sagher O. Transorbital penetrating injury: Case series, review of the literature, and proposed management algorithm. Journal of Neurosurgery 2011;114:53–61. 2. Kothari K, Singh AK, Das S. Penetrating skull injury with six inch fence rod. National Journal of Maxillofacical Surgery 2012;3: 207–210. 3. Syrmos N, Ganau M, De Carlo A, Prisco L, Ganau L, Valadakis V, Grigoriou K, Iliadis C, Arvanitakis D. Dealing with the surgical and medical challenges of penetrating brain injuries. Case Reports in Surgery 2013. 4. Selvanathan S, Goldschlager T, McMillen J, Campbell S. Penetrating craniocerebral injuries from nail-gun use. Journal of Clinical Neuroscience 2007;14:678–683. 5. Aarabi B, Alden TD, Chestnut RM, et al. Management and prognosis of penetrating brain injury—guidelines. J Trauma 2001; 51(Suppl):S1–86. 6. Kieck CF, de Villiers JC. Vascular-lesions due to transcranial stab wounds. Journal of Neurosurgery 1984;60:42–46. 7. Azarpira N, Pourjafar M, Neghad MN. Penetrating knife injury to the temporal lobe: A case report. Neurosurgery Quarterly 2013;23: 64–65. 8. Karim T, Topno M. An unusual case of penetrating head injury in a child. Journal of Emergencies, Trauma & Shock 2010;3:197–198. 9. Kazim SF, Shamim MS, Tahir MZ, Enam SA, Waheed S. Management of penetrating brain injury. Journal of Emergencies, Trauma & Shock 2011;4:395–402.
DOI: 10.3109/02699052.2014.934284
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