252 Escobedo et al
World J Emerg Med, Vol 4, No 4, 2013
Review Article
Traumatic brain injury: A case-based review Liza Victoria S Escobedo1, Joseph Habboushe1, Haytham Kaafarani2, George Velmahos2, Kaushal Shah3, Jarone Lee2 1
Department of Emergency Medicine, Beth Israel Medical Center, New York, NY, USA Trauma, Emergency Surgery, Surgical Critical Care, Massachusetts General Hospital, Boston, MA, USA 3 Department of Emergency Medicine, Mount Sinai School of Medicine, New York, NY, USA 2
Corresponding Author: Jarone Lee, Email: [email protected]
BACKGROUND: Traumatic brain injuries are common and costly to hospital systems. Most of the guidelines on management of traumatic brain injuries are taken from the Brain Trauma Foundation Guidelines. This is a review of the current literature discussing the evolving practice of traumatic brain injury. DATA SOURCES: A literature search using multiple databases was performed for articles published through September 2012 with concentration on meta-analyses, systematic reviews, and randomized controlled trials. RESULTS: The focus of care should be to minimize secondary brain injury by surgically decompressing certain hematomas, maintain systolic blood pressure above 90 mmHg, oxygen saturations above 93%, euthermia, intracranial pressures below 20 mmHg, and cerebral perfusion pressure between 60–80 mmHg. CONCLUSION: Much is still unknown about the management of traumatic brain injury. The current practice guidelines have not yet been sufficiently validated, however equipoise is a major issue when conducting randomized control trials among patients with traumatic brain injury. KEY WORDS: Traumatic brain injury; Emergency departments; Glascow Coma Scale World J Emerg Med 2013;4(4):252–259 DOI: 10.5847/ wjem.j.issn.1920–8642.2013.04.002
BACKGROUND Over 1.7 million people present to US emergency departments (EDs) after sustaining traumatic brain injury (TBI) each year.[1] Of those, approximately 52 000 will die, 275 000 are hospitalized, and 1.4 million are evaluated and discharged from an EDs.[1] Distribution of age is trimodal with predominance in the age groups of: 0–4 years; 15–19 years; and >65 years. The most common cause is falls followed by motor vehicle crashes and assaults. In the United States, cost of care, which includes loss of productivity, was estimated to be $76.5 billion in 2000.[1] TBI can occur as an isolated injury or as part of multisystem trauma. When compared to other traumatic injuries, survivors of TBI tend to be left with greater neurologic disability and functional limitations.[2] Much of the existing medical practice guidelines on TBI are www.wjem.org © 2013 World Journal of Emergency Medicine
based on the Brain Trauma Foundation Guidelines.[3] This is a review of the current literature discussing the evolving practice of TBI. TBI is defined as impaired brain function as a result of mechanical force, most commonly caused by blunt force. Severity is based on the level of consciousness as defined by the Glascow Coma Scale (GCS) not by the actual brain lesion. Mild TBI can be seen in patients presenting with a GCS of 14–15, with moderate and severe presenting with a GCS 9–13 and 3–8, respectively Brain injury is defined as primary and secondary. Primary injury is damage to brain parenchyma as a result of the initial injury. It is nonreversible and the prevention of secondary injury is the goal of management. Secondary injury occurs hours to days later as a result of the inflammatory cascade that causes cerebral edema and cell death. Secondary brain
World J Emerg Med, Vol 4, No 4, 2013
injury can be minimized by preventing and correcting hypoxemia, hypotension, anemia, hypoglycemia, and hyperthermia, and by evacuating certain intracranial masses. [4–6] Prehospital and inpatient hypoxemia, pyrexia, and hypotension are independent predictors of mortality and disability.[7] One prospective trial found that a single episode of hypotension with a systolic blood pressure 90 mmHg, and preventing hypoxemia with a goal PaO2 >60 mmHg or O2 saturation >93%.[11]
Airway management Airway assessment and management is the first priority. While the current literature cites opposing arguments for whether the TBI patient requiring airway control should be intubated in the prehospital setting or in the hospital,[12–14] some pre-hospital systems have moved away from prehospital intubation. This is not because of difficulty in securing the airway prehospital, but because of poor outcomes with over-ventilation.[14] Indications for intubating the TBI patient are similar to usual reasons for intubation and include inability to oxygenate, ventilate, and protect the airway or worsening status with expectations of needing airway support. While coma (i.e. GCS40 Unilateral or bilateral motor posturing Systolic blood pressure 15 mm Hematoma volume >30 cm3 regardless of GCS Subdural hematoma (SDH) SDH larger than 5 mm on CT Hematoma thickness >10 mm Midline shift > 5 mm GCS 20 mmHg Asymmetric or fixed and dilated pupils Intraparenchymal lesions Progressive neurologic deterioration Failed medical management with CT evidence of mass effect GCS 6–8 with frontal or temporal contusions >20 cm3 and midline shift of >5 mm or cisternal compression on CT Hematoma volume >50 cm3 Posterior fossa lesions Mass effect on CT Neurologic deterioration Depressed skull fractures Skull depression >1 cm Frontal sinus involvement Dural penetration Associated intracranial hematoma Gross cosmetic deformity Infection or obvious contamination Pneumocephalus
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persistently elevated ICPs despite aggressive therapy. There are few studies on decompressive craniectomy in TBI. Most of the recommendations are borrowed from craniectomy among patients with malignant strokes. A few meta-analyses found lower mortalities and favorable outcomes with ICP monitoring and decompressive craniotomy. [54,55] Even at advanced age >80 years, aggressive treatment was still more cost-effective though the impact was less.[56] However, a recent randomized controlled trial found that early bifrontal decompressive craniectomy for refractory ICP elevations resulted in lower ICPs, and decreased the length of ICU stay but at the expense of more unfavorable neurologic outcomes.[57]
Therapeutic hypothermia Prophylactic hypothermia has been shown in animal studies and small retrospective human studies to improve outcomes, but has not shown benefit in large prospective human studies. [58–60] The use of hypothermia remains controversial and is not currently supported by multiple meta-analysis showing potential harm.[52,53] However, hypothermia has been used as salvage therapy for patients with persistently elevated ICPs resistant to all other treatments. Author’s recommendation Patients presenting to the ED with a history of head trauma should be assumed to have significant injury until otherwise determined, either by clinical examination or imaging. Initial work-up including history, physical examination, and diagnostic imaging as needed should be thorough and complete. We recommend that treatment of TBI be guided by the clinical situation utilizing the GCS to grade severity. Management of moderate TBI patients is casedependent but will likely be similar to that of severe TBI. Generally, the patient with a persistent GCS of 13 or less may require admission and observation. A small percentage may worsen from increasing ICP. What may present as a moderate TBI may quickly convert to a severe TBI even in the absence of risk factors. Severe TBI patients should be stabilized and have rapid neurosurgical consultation. Diagnostic imaging with CT should be performed promptly to quantify the extent of injury and need for intervention. Aggressive therapy should be started immediately to reduce secondary injury (Table 3). Coagulation studies should be ordered in patients on chronic anticoagulation or who may be at risk for increased bleeding such as malignancy, hemophilia, von Willebrand's disease, or
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Table 3. Authors recommendations Emergency neurosurgical evaluation for surgical decompression of certain hematomas Maintain ICP 90 mmHg Avoid hypotonic fluids and albumin for resuscitation Oxygen saturation above 93% or PaO2 >60 mmHg Euthermia Maintain normal PaCO2 (35–40 mmHg) Seizure prophylaxis for first week post-injury
257
Funding: None. Ethical approval: This study was approved by the institutional ethics Committees. Conflicts of interest: We have no conflicts of interest to report. Contributors: Escobedo LVS proposed the study and wrote the paper. All authors contributed to the design and interpretation of the study and to further drafts.
REFERENCES
Subarachnoid Intraparenchymal Skull fracture Epidural
Subdural
Diffuse axonal injury
Figure 1. Epidural Hematoma (EDH): Lenticular-shaped hemorrhage that does not cross suture lines. The hemorrhage caused most commonly by injury to the middle meningeal artery. Collection of blood between the dura mater and cranium is classically associated with a lucid interval followed by unconsciousness. Subdural hematoma (SDH): Cresent-shaped hemorrhage that crosses suture lines secondary to shearing of bridging veins between the dura and arachnoid space. Classic presentation includes gradually increasing headache and confusion after head injury. Diffuse axonal injury (DAI): MRI preferred diagnostic modality given that over half of CT scans of patients with DAI are normal on presentation. When present on CT, it appears as multiple ovoidshaped petechial hemorrhages at gray-white junction, typically bilateral, resulting from the breaking of axons from the neuronal body. Frequently, DAI involves the frontal and temporal lobes, corpus callosum, caudate nuclei, thalamus, tegmentum, and internal capsule. Intraparenchymal hemorrhage (IPH): Collection of blood in the cerebral parenchyma. Acute hemorrhage in traumatic brain injury appears hyperdense, whereas subacute and chronic appear isodense and hypodense respectively.
other congenital coagulation disorders. Anticoagulation should be reversed as soon as possible. All patients with severe TBI should receive seizure prophylaxis with phenytoin or levetiracetam for the first week post-injury (level II evidence). For elevated ICPs, we ensure that the patient is well sedated, the head of bed is elevated, and jugular veins are straight. If the ICP remains persistently elevated, we consider osmotic therapy and salvage therapies, such as surgical decompression.
1 Faul M XL, Wald MM, Coronado VG. Traumatic Brain Injury in the United States: Emergency Department Visits, Hospitalizations and Deaths 2002–2006, 2010, Center for Disease Control and Prevention, National Center for Injury Prevention and Control: Atlanta, GA. 2 Lannoo E, Van Rietvelde F, Colardyn F, Lemmerling M, Vandekerckhove T, Jannes C, et al. Early predictors of mortality and morbidity after severe closed head injury. J Neurotrauma 2000; 17: 403–414. 3 Kochanek PM, Carney N, Adelson PD, Ashwal S, Bell MJ, Bratton S, et al. Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents—second edition. Pediatr Crit Care Med 2012; 13 Suppl 1: S1–82. 4 Rosonke S, Legome E. Head trauma. J Emerg Med 2006 ; 31: 421–425. 5 Reaven NL, Lovett JE, Funk SE. Brain injury and fever: hospital length of stay and cost outcomes. J Intensive Care Med 2009; 24: 131–139. 6 Greer DM, Funk SE, Reaven NL, Ouzounelli M, Uman GC. Impact of fever on outcome in patients with stroke and neurologic injury: a comprehensive meta-analysis. Stroke 2008; 39: 3029–3035. 7 Jones PA, Andrews PJ, Midgley S, Anderson SI, Piper IR, Tocher JL, et al. Measuring the burden of secondary insults in headinjured patients during intensive care. J Neurosurg Anesthesiol 1994; 6: 4–14. 8 Chesnut RM, Marshall LF, Klauber MR, Blunt BA, Baldwin N, Eisenberg HM, et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma 1993; 34: 216–222. 9 Langham J, Goldfrad C, Teasdale G, Shaw D, Rowan K. Calcium channel blockers for acute traumatic brain injury. Cochrane Database Syst Rev 2003; (4): CD000565. 10 Ker K, Perel P, Blackhall K, Roberts I. How effective are some common treatments for traumatic brain injury? BMJ 2008; 337: a865. 11 Murray GD, Butcher I, McHugh GS, Lu J, Mushkudiani NA, Maas AI, et al. Multivariable prognostic analysis in traumatic brain injury: results from the IMPACT study. J Neurotrauma 2007; 24: 329–337. 12 Bukur M, Kurtovic S, Berry C, Tanios M, Margulies DR, Ley EJ, et al. Pre-hospital intubation is associated with increased mortality after traumatic brain injury. J Surg Res 2011; 170: 117–121. 13 Bernard SA, Nguyen V, Cameron P, Masci K, Fitzgerald M, Cooper DJ, et al. Prehospital rapid sequence intubation improves functional outcome for patients with severe traumatic brain injury: a randomized controlled trial. Ann Surg 2010; 252: 959– www.wjem.org
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965. 14 Davis DP, Hoyt DB, Ochs M, Fortlage D, Holbrook T, Marshall LK, et al. The effect of paramedic rapid sequence intubation on outcome in patients with severe traumatic brain injury. J Trauma 2003; 54: 444–453. 15 Moss E, Powell D, Gibson RM, McDowall DG. Effect of etomidate on intracranial pressure and cerebral perfusion pressure. Br J Anaesth 1979; 51: 347–352. 16 Hughes S. Towards evidence based emergency medicine: best BETs from the Manchester Royal Infirmary. BET 3: is ketamine a viable induction agent for the trauma patient with potential brain injury. Emerg Med J 2011; 28: 1076–1077. 17 Clancy M, Halford S, Walls R, Murphy M. In patients with head injuries who undergo rapid sequence intubation using succinylcholine, does pretreatment with a competitive neuromuscular blocking agent improve outcome? A literature review. Emerg Med J 2001; 18: 373–375. 18 Kerr ME, Sereika SM, Orndoff P, Weber B, Rudy EB, Marion D, et al. Effect of neuromuscular blockers and opiates on the cerebrovascular response to endotracheal suctioning in adults with severe head injuries. Am J Crit Care 1998; 7: 205–217. 19 Salhi B, Stettner E. In defense of the use of lidocaine in rapid sequence intubation. Ann Emerg Med 2007; 49: 84–86. 20 Vaillancourt C, Kapur AK. Opposition to the use of lidocaine in rapid sequence intubation. Ann Emerg Med 2007; 49: 86–87. 21 Manoach S, Paladino L. Manual in-line stabilization for acute airway management of suspected cervical spine injury: historical review and current questions. Ann Emerg Med 2007; 50: 236– 245. 22 Robitaille A, Williams SR, Tremblay MH, Guilbert F, Thériault M, Drolet P. Cervical spine motion during tracheal intubation with manual in-line stabilization: direct laryngoscopy versus GlideScope videolaryngoscopy. Anesth Analg 2008; 106: 935– 941. 23 Mosier JM, Stolz U, Chiu S, Sakles JC. Difficult airway management in the emergency department: GlideScope videolaryngoscopy compared to direct laryngoscopy. J Emerg Med 2012; 42: 629–634. 24 Sakles JC, Mosier JM, Chiu S, Keim SM. Tracheal intubation in the emergency department: a comparison of GlideScope(R) video laryngoscopy to direct laryngoscopy in 822 intubations. J Emerg Med 2012; 42: 400–405. 25 Griesdale DE, Liu D, McKinney J, Choi PT. Glidescope® video-laryngoscopy versus direct laryngoscopy for endotracheal intubation: a systematic review and meta-analysis. Can J Anaesth 2012; 59: 41–52. 26 Badri S, Chen J, Barber J, Temkin NR, Dikmen SS, Chesnut RM, et al. Mortality and long-term functional outcome associated with intracranial pressure after traumatic brain injury. Intensive Care Med 2012; 38: 1800–1809. 27 Wakai A, McCabe A, Roberts I, Schierhout G. Mannitol for acute traumatic brain injury. Cochrane Database Syst Rev 2013; 8: CD001049. 28 Fink ME. Osmotherapy for intracranial hypertension: mannitol versus hypertonic saline. Continuum (Minneap Minn) 2012; 18: 640–654. 29 Schierhout G, Roberts I. The Cochrane Brain and Spinal Cord Injury Group. J Neurol Neurosurg Psychiatry 1997; 63: 1–3. 30 Brain Trauma Foundation; American Association of Neurological www.wjem.org
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Surgeons; Congress of Neurological Surgeons; Joint Section on Neurotrauma and Critical Care, AANS/CNS, Carney NA, et al. Guidelines for the management of severe traumatic brain injury. Introduction. J Neurotrauma 2007; 24 Suppl 1: S1–2. Finfer S, Bellomo R, Boyce N, French J, Myburgh J, Norton R, et al. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med 2004; 350: 2247–256. Stein SC, Fabbri A, Servadei F, Glick HA. A critical comparison of clinical decision instruments for computed tomographic scanning in mild closed traumatic brain injury in adolescents and adults. Ann Emerg Med 2009; 53: 180–188. Melnick ER, Szlezak CM, Bentley SK, Dziura JD, Kotlyar S, Post LA. CT overuse for mild traumatic brain injury. Jt Comm J Qual Patient Saf 2012; 38: 483–489. Eagles D, Stiell IG, Clement CM, Brehaut J, Taljaard M, Kelly AM, et al. International survey of emergency physicians' awareness and use of the Canadian Cervical-Spine Rule and the Canadian Computed Tomography Head Rule. Acad Emerg Med 2008; 15: 1256–1261. Smits M, Dippel DW, Steyerberg EW, de Haan GG, Dekker HM, Vos PE, et al. Predicting intracranial traumatic findings on computed tomography in patients with minor head injury: the CHIP prediction rule. Ann Intern Med 2007; 146: 397–405. Brown CV, Weng J, Oh D, Salim A, Kasotakis G, Demetriades D, et al. Does routine serial computed tomography of the head influence management of traumatic brain injury? A prospective evaluation. J Trauma 2004; 57: 939–943. Sperry JL, Gentilello LM, Minei JP, Diaz-Arrastia RR, Friese RS, Shafi S. Waiting for the patient to "sober up": Effect of alcohol intoxication on glasgow coma scale score of brain injured patients. J Trauma 2006; 61: 1305–1311. Godbout BJ, Lee J, Newman DH, Bodle EE, Shah K. Yield of head CT in the alcohol-intoxicated patient in the emergency department. Emerg Radiol 2011; 18: 381–384. Lee J, Evans CS, Singh N, Kirschner J, Runde D, Newman D, et al. Head computed tomography utilization and intracranial hemorrhage rates. Emerg Radiol 2013; 20: 219–223. Downey DM, Monson B, Butler KL, Fortuna GR Jr, Saxe JM, Dolan JP, et al. Does platelet administration affect mortality in elderly head-injured patients taking antiplatelet medications? Am Surg 2009; 75: 1100–1103. Nishijima DK, Zehtabchi S, Berrong J, Legome E. Utility of platelet transfusion in adult patients with traumatic intracranial hemorrhage and preinjury antiplatelet use: a systematic review. J Trauma Acute Care Surg 2012; 72: 1658–1663. Ivascu FA, Howells GA, Junn FS, Bair HA, Bendick PJ, Janczyk RJ. Rapid warfarin reversal in anticoagulated patients with traumatic intracranial hemorrhage reduces hemorrhage progression and mortality. J Trauma 2005; 59: 1131–1137; discussion 1137–1139. Edwards P, Arango M, Balica L, Cottingham R, El-Sayed H, Farrell B, et al. Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticosteroid in adults with head injury-outcomes at 6 months. Lancet 2005; 365: 1957–1959. Roberts I, Shakur H, Ker K, Coats T; CRASH-2 Trial collaborators. Antifibrinolytic drugs for acute traumatic injury. Cochrane Database Syst Rev 2011; (1): CD004896. Yank V, Tuohy CV, Logan AC, Bravata DM, Staudenmayer K,
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Eisenhut R, et al. Systematic review: benefits and harms of inhospital use of recombinant factor VIIa for off-label indications. Ann Intern Med 2011; 154: 529–540. Diringer MN, Skolnick BE, Mayer SA, Steiner T, Davis SM, Brun NC, et al. Thromboembolic events with recombinant activated factor VII in spontaneous intracerebral hemorrhage: results from the Factor Seven for Acute Hemorrhagic Stroke (FAST) trial. Stroke 2010; 41: 48–53. Schierhout G, Roberts I. WITHDRAWN: Antiepileptic drugs for preventing seizures following acute traumatic brain injury. Cochrane Database Syst Rev 2012; 6: CD000173. Temkin NR, Dikmen SS, Anderson GD, Wilensky AJ, Holmes MD, Cohen W, et al. Valproate therapy for prevention of posttraumatic seizures: a randomized trial. J Neurosurg 1999; 91: 593–600. Chang BS, Lowenstein DH; Quality Standards Subcommittee of the American Academy of Neurology. Practice parameter: antiepileptic drug prophylaxis in severe traumatic brain injury: report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2003; 60: 10–16. Darrah SD, Chuang J, Mohler LM, Chen X, Cummings EE, Burnett T, et al. Dilantin therapy in an experimental model of traumatic brain injury: effects of limited versus daily treatment on neurological and behavioral recovery. J Neurotrauma 2011; 28: 43–55. Pieracci FM, Moore EE, Beauchamp K, Tebockhorst S, Barnett CC, Bensard DD, et al. A cost-minimization analysis of phenytoin versus levetiracetam for early seizure pharmacoprophylaxis after traumatic brain injury. J Trauma Acute Care Surg 2012; 72: 276–281. Coester A, Neumann CR, Schmidt MI. Intensive insulin therapy in severe traumatic brain injury: a randomized trial. J Trauma 2010; 68: 904–911.
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53 Yang M, Guo Q, Zhang X, Sun S, Wang Y, Zhao L, et al. Intensive insulin therapy on infection rate, days in NICU, inhospital mortality and neurological outcome in severe traumatic brain injury patients: a randomized controlled trial. Int J Nurs Stud 2009; 46: 753–758. 54 Bor-Seng-Shu E, Figueiredo EG, Amorim RL, Teixeira MJ, Valbuza JS, de Oliveira MM, et al. Decompressive craniectomy: a meta-analysis of influences on intracranial pressure and cerebral perfusion pressure in the treatment of traumatic brain injury. J Neurosurg 2012; 117: 589–596. 55 Sahuquillo J, Arikan F. Decompressive craniectomy for the treatment of refractory high intracranial pressure in traumatic brain injury. Cochrane Database Syst Rev 2006; (1): CD003983. 56 Whitmore RG, Thawani JP, Grady MS, Levine JM, Sanborn MR, Stein SC. Is aggressive treatment of traumatic brain injury cost-effective? J Neurosurg 2012; 116: 1106–1113. 57 Timmons SD, Ullman JS, Eisenberg HM. Craniectomy in diffuse traumatic brain injury. N Engl J Med 2011; 365: 373; author reply 376. 58 Harris OA, Colford JM Jr, Good MC, Matz PG. The role of hypothermia in the management of severe brain injury: a metaanalysis. Arch Neurol 2002; 59: 1077–1083. 59 Sydenham E, Roberts I, Alderson P. Hypothermia for traumatic head injury. Cochrane Database Syst Rev 2009; (2): CD001048. 60 Clifton GL, Valadka A, Zygun D, Coffey CS, Drever P, Fourwinds S, et al. Very early hypothermia induction in patients with severe brain injury (the National Acute Brain Injury Study: Hypothermia II): a randomised trial. Lancet Neurol 2011; 10: 131–139.
Received April 15, 2013 Accepted after revision October 11, 2013
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World J Emerg Med, Vol 4, No 4, 2013
Review Article
Traumatic brain injury: A case-based review Liza Victoria S Escobedo1, Joseph Habboushe1, Haytham Kaafarani2, George Velmahos2, Kaushal Shah3, Jarone Lee2 1
Department of Emergency Medicine, Beth Israel Medical Center, New York, NY, USA Trauma, Emergency Surgery, Surgical Critical Care, Massachusetts General Hospital, Boston, MA, USA 3 Department of Emergency Medicine, Mount Sinai School of Medicine, New York, NY, USA 2
Corresponding Author: Jarone Lee, Email: [email protected]
BACKGROUND: Traumatic brain injuries are common and costly to hospital systems. Most of the guidelines on management of traumatic brain injuries are taken from the Brain Trauma Foundation Guidelines. This is a review of the current literature discussing the evolving practice of traumatic brain injury. DATA SOURCES: A literature search using multiple databases was performed for articles published through September 2012 with concentration on meta-analyses, systematic reviews, and randomized controlled trials. RESULTS: The focus of care should be to minimize secondary brain injury by surgically decompressing certain hematomas, maintain systolic blood pressure above 90 mmHg, oxygen saturations above 93%, euthermia, intracranial pressures below 20 mmHg, and cerebral perfusion pressure between 60–80 mmHg. CONCLUSION: Much is still unknown about the management of traumatic brain injury. The current practice guidelines have not yet been sufficiently validated, however equipoise is a major issue when conducting randomized control trials among patients with traumatic brain injury. KEY WORDS: Traumatic brain injury; Emergency departments; Glascow Coma Scale World J Emerg Med 2013;4(4):252–259 DOI: 10.5847/ wjem.j.issn.1920–8642.2013.04.002
BACKGROUND Over 1.7 million people present to US emergency departments (EDs) after sustaining traumatic brain injury (TBI) each year.[1] Of those, approximately 52 000 will die, 275 000 are hospitalized, and 1.4 million are evaluated and discharged from an EDs.[1] Distribution of age is trimodal with predominance in the age groups of: 0–4 years; 15–19 years; and >65 years. The most common cause is falls followed by motor vehicle crashes and assaults. In the United States, cost of care, which includes loss of productivity, was estimated to be $76.5 billion in 2000.[1] TBI can occur as an isolated injury or as part of multisystem trauma. When compared to other traumatic injuries, survivors of TBI tend to be left with greater neurologic disability and functional limitations.[2] Much of the existing medical practice guidelines on TBI are www.wjem.org © 2013 World Journal of Emergency Medicine
based on the Brain Trauma Foundation Guidelines.[3] This is a review of the current literature discussing the evolving practice of TBI. TBI is defined as impaired brain function as a result of mechanical force, most commonly caused by blunt force. Severity is based on the level of consciousness as defined by the Glascow Coma Scale (GCS) not by the actual brain lesion. Mild TBI can be seen in patients presenting with a GCS of 14–15, with moderate and severe presenting with a GCS 9–13 and 3–8, respectively Brain injury is defined as primary and secondary. Primary injury is damage to brain parenchyma as a result of the initial injury. It is nonreversible and the prevention of secondary injury is the goal of management. Secondary injury occurs hours to days later as a result of the inflammatory cascade that causes cerebral edema and cell death. Secondary brain
World J Emerg Med, Vol 4, No 4, 2013
injury can be minimized by preventing and correcting hypoxemia, hypotension, anemia, hypoglycemia, and hyperthermia, and by evacuating certain intracranial masses. [4–6] Prehospital and inpatient hypoxemia, pyrexia, and hypotension are independent predictors of mortality and disability.[7] One prospective trial found that a single episode of hypotension with a systolic blood pressure 90 mmHg, and preventing hypoxemia with a goal PaO2 >60 mmHg or O2 saturation >93%.[11]
Airway management Airway assessment and management is the first priority. While the current literature cites opposing arguments for whether the TBI patient requiring airway control should be intubated in the prehospital setting or in the hospital,[12–14] some pre-hospital systems have moved away from prehospital intubation. This is not because of difficulty in securing the airway prehospital, but because of poor outcomes with over-ventilation.[14] Indications for intubating the TBI patient are similar to usual reasons for intubation and include inability to oxygenate, ventilate, and protect the airway or worsening status with expectations of needing airway support. While coma (i.e. GCS40 Unilateral or bilateral motor posturing Systolic blood pressure 15 mm Hematoma volume >30 cm3 regardless of GCS Subdural hematoma (SDH) SDH larger than 5 mm on CT Hematoma thickness >10 mm Midline shift > 5 mm GCS 20 mmHg Asymmetric or fixed and dilated pupils Intraparenchymal lesions Progressive neurologic deterioration Failed medical management with CT evidence of mass effect GCS 6–8 with frontal or temporal contusions >20 cm3 and midline shift of >5 mm or cisternal compression on CT Hematoma volume >50 cm3 Posterior fossa lesions Mass effect on CT Neurologic deterioration Depressed skull fractures Skull depression >1 cm Frontal sinus involvement Dural penetration Associated intracranial hematoma Gross cosmetic deformity Infection or obvious contamination Pneumocephalus
www.wjem.org
World J Emerg Med, Vol 4, No 4, 2013
persistently elevated ICPs despite aggressive therapy. There are few studies on decompressive craniectomy in TBI. Most of the recommendations are borrowed from craniectomy among patients with malignant strokes. A few meta-analyses found lower mortalities and favorable outcomes with ICP monitoring and decompressive craniotomy. [54,55] Even at advanced age >80 years, aggressive treatment was still more cost-effective though the impact was less.[56] However, a recent randomized controlled trial found that early bifrontal decompressive craniectomy for refractory ICP elevations resulted in lower ICPs, and decreased the length of ICU stay but at the expense of more unfavorable neurologic outcomes.[57]
Therapeutic hypothermia Prophylactic hypothermia has been shown in animal studies and small retrospective human studies to improve outcomes, but has not shown benefit in large prospective human studies. [58–60] The use of hypothermia remains controversial and is not currently supported by multiple meta-analysis showing potential harm.[52,53] However, hypothermia has been used as salvage therapy for patients with persistently elevated ICPs resistant to all other treatments. Author’s recommendation Patients presenting to the ED with a history of head trauma should be assumed to have significant injury until otherwise determined, either by clinical examination or imaging. Initial work-up including history, physical examination, and diagnostic imaging as needed should be thorough and complete. We recommend that treatment of TBI be guided by the clinical situation utilizing the GCS to grade severity. Management of moderate TBI patients is casedependent but will likely be similar to that of severe TBI. Generally, the patient with a persistent GCS of 13 or less may require admission and observation. A small percentage may worsen from increasing ICP. What may present as a moderate TBI may quickly convert to a severe TBI even in the absence of risk factors. Severe TBI patients should be stabilized and have rapid neurosurgical consultation. Diagnostic imaging with CT should be performed promptly to quantify the extent of injury and need for intervention. Aggressive therapy should be started immediately to reduce secondary injury (Table 3). Coagulation studies should be ordered in patients on chronic anticoagulation or who may be at risk for increased bleeding such as malignancy, hemophilia, von Willebrand's disease, or
World J Emerg Med, Vol 4, No 4, 2013
Table 3. Authors recommendations Emergency neurosurgical evaluation for surgical decompression of certain hematomas Maintain ICP 90 mmHg Avoid hypotonic fluids and albumin for resuscitation Oxygen saturation above 93% or PaO2 >60 mmHg Euthermia Maintain normal PaCO2 (35–40 mmHg) Seizure prophylaxis for first week post-injury
257
Funding: None. Ethical approval: This study was approved by the institutional ethics Committees. Conflicts of interest: We have no conflicts of interest to report. Contributors: Escobedo LVS proposed the study and wrote the paper. All authors contributed to the design and interpretation of the study and to further drafts.
REFERENCES
Subarachnoid Intraparenchymal Skull fracture Epidural
Subdural
Diffuse axonal injury
Figure 1. Epidural Hematoma (EDH): Lenticular-shaped hemorrhage that does not cross suture lines. The hemorrhage caused most commonly by injury to the middle meningeal artery. Collection of blood between the dura mater and cranium is classically associated with a lucid interval followed by unconsciousness. Subdural hematoma (SDH): Cresent-shaped hemorrhage that crosses suture lines secondary to shearing of bridging veins between the dura and arachnoid space. Classic presentation includes gradually increasing headache and confusion after head injury. Diffuse axonal injury (DAI): MRI preferred diagnostic modality given that over half of CT scans of patients with DAI are normal on presentation. When present on CT, it appears as multiple ovoidshaped petechial hemorrhages at gray-white junction, typically bilateral, resulting from the breaking of axons from the neuronal body. Frequently, DAI involves the frontal and temporal lobes, corpus callosum, caudate nuclei, thalamus, tegmentum, and internal capsule. Intraparenchymal hemorrhage (IPH): Collection of blood in the cerebral parenchyma. Acute hemorrhage in traumatic brain injury appears hyperdense, whereas subacute and chronic appear isodense and hypodense respectively.
other congenital coagulation disorders. Anticoagulation should be reversed as soon as possible. All patients with severe TBI should receive seizure prophylaxis with phenytoin or levetiracetam for the first week post-injury (level II evidence). For elevated ICPs, we ensure that the patient is well sedated, the head of bed is elevated, and jugular veins are straight. If the ICP remains persistently elevated, we consider osmotic therapy and salvage therapies, such as surgical decompression.
1 Faul M XL, Wald MM, Coronado VG. Traumatic Brain Injury in the United States: Emergency Department Visits, Hospitalizations and Deaths 2002–2006, 2010, Center for Disease Control and Prevention, National Center for Injury Prevention and Control: Atlanta, GA. 2 Lannoo E, Van Rietvelde F, Colardyn F, Lemmerling M, Vandekerckhove T, Jannes C, et al. Early predictors of mortality and morbidity after severe closed head injury. J Neurotrauma 2000; 17: 403–414. 3 Kochanek PM, Carney N, Adelson PD, Ashwal S, Bell MJ, Bratton S, et al. Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents—second edition. Pediatr Crit Care Med 2012; 13 Suppl 1: S1–82. 4 Rosonke S, Legome E. Head trauma. J Emerg Med 2006 ; 31: 421–425. 5 Reaven NL, Lovett JE, Funk SE. Brain injury and fever: hospital length of stay and cost outcomes. J Intensive Care Med 2009; 24: 131–139. 6 Greer DM, Funk SE, Reaven NL, Ouzounelli M, Uman GC. Impact of fever on outcome in patients with stroke and neurologic injury: a comprehensive meta-analysis. Stroke 2008; 39: 3029–3035. 7 Jones PA, Andrews PJ, Midgley S, Anderson SI, Piper IR, Tocher JL, et al. Measuring the burden of secondary insults in headinjured patients during intensive care. J Neurosurg Anesthesiol 1994; 6: 4–14. 8 Chesnut RM, Marshall LF, Klauber MR, Blunt BA, Baldwin N, Eisenberg HM, et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma 1993; 34: 216–222. 9 Langham J, Goldfrad C, Teasdale G, Shaw D, Rowan K. Calcium channel blockers for acute traumatic brain injury. Cochrane Database Syst Rev 2003; (4): CD000565. 10 Ker K, Perel P, Blackhall K, Roberts I. How effective are some common treatments for traumatic brain injury? BMJ 2008; 337: a865. 11 Murray GD, Butcher I, McHugh GS, Lu J, Mushkudiani NA, Maas AI, et al. Multivariable prognostic analysis in traumatic brain injury: results from the IMPACT study. J Neurotrauma 2007; 24: 329–337. 12 Bukur M, Kurtovic S, Berry C, Tanios M, Margulies DR, Ley EJ, et al. Pre-hospital intubation is associated with increased mortality after traumatic brain injury. J Surg Res 2011; 170: 117–121. 13 Bernard SA, Nguyen V, Cameron P, Masci K, Fitzgerald M, Cooper DJ, et al. Prehospital rapid sequence intubation improves functional outcome for patients with severe traumatic brain injury: a randomized controlled trial. Ann Surg 2010; 252: 959– www.wjem.org
258 Escobedo et al
965. 14 Davis DP, Hoyt DB, Ochs M, Fortlage D, Holbrook T, Marshall LK, et al. The effect of paramedic rapid sequence intubation on outcome in patients with severe traumatic brain injury. J Trauma 2003; 54: 444–453. 15 Moss E, Powell D, Gibson RM, McDowall DG. Effect of etomidate on intracranial pressure and cerebral perfusion pressure. Br J Anaesth 1979; 51: 347–352. 16 Hughes S. Towards evidence based emergency medicine: best BETs from the Manchester Royal Infirmary. BET 3: is ketamine a viable induction agent for the trauma patient with potential brain injury. Emerg Med J 2011; 28: 1076–1077. 17 Clancy M, Halford S, Walls R, Murphy M. In patients with head injuries who undergo rapid sequence intubation using succinylcholine, does pretreatment with a competitive neuromuscular blocking agent improve outcome? A literature review. Emerg Med J 2001; 18: 373–375. 18 Kerr ME, Sereika SM, Orndoff P, Weber B, Rudy EB, Marion D, et al. Effect of neuromuscular blockers and opiates on the cerebrovascular response to endotracheal suctioning in adults with severe head injuries. Am J Crit Care 1998; 7: 205–217. 19 Salhi B, Stettner E. In defense of the use of lidocaine in rapid sequence intubation. Ann Emerg Med 2007; 49: 84–86. 20 Vaillancourt C, Kapur AK. Opposition to the use of lidocaine in rapid sequence intubation. Ann Emerg Med 2007; 49: 86–87. 21 Manoach S, Paladino L. Manual in-line stabilization for acute airway management of suspected cervical spine injury: historical review and current questions. Ann Emerg Med 2007; 50: 236– 245. 22 Robitaille A, Williams SR, Tremblay MH, Guilbert F, Thériault M, Drolet P. Cervical spine motion during tracheal intubation with manual in-line stabilization: direct laryngoscopy versus GlideScope videolaryngoscopy. Anesth Analg 2008; 106: 935– 941. 23 Mosier JM, Stolz U, Chiu S, Sakles JC. Difficult airway management in the emergency department: GlideScope videolaryngoscopy compared to direct laryngoscopy. J Emerg Med 2012; 42: 629–634. 24 Sakles JC, Mosier JM, Chiu S, Keim SM. Tracheal intubation in the emergency department: a comparison of GlideScope(R) video laryngoscopy to direct laryngoscopy in 822 intubations. J Emerg Med 2012; 42: 400–405. 25 Griesdale DE, Liu D, McKinney J, Choi PT. Glidescope® video-laryngoscopy versus direct laryngoscopy for endotracheal intubation: a systematic review and meta-analysis. Can J Anaesth 2012; 59: 41–52. 26 Badri S, Chen J, Barber J, Temkin NR, Dikmen SS, Chesnut RM, et al. Mortality and long-term functional outcome associated with intracranial pressure after traumatic brain injury. Intensive Care Med 2012; 38: 1800–1809. 27 Wakai A, McCabe A, Roberts I, Schierhout G. Mannitol for acute traumatic brain injury. Cochrane Database Syst Rev 2013; 8: CD001049. 28 Fink ME. Osmotherapy for intracranial hypertension: mannitol versus hypertonic saline. Continuum (Minneap Minn) 2012; 18: 640–654. 29 Schierhout G, Roberts I. The Cochrane Brain and Spinal Cord Injury Group. J Neurol Neurosurg Psychiatry 1997; 63: 1–3. 30 Brain Trauma Foundation; American Association of Neurological www.wjem.org
World J Emerg Med, Vol 4, No 4, 2013
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
Surgeons; Congress of Neurological Surgeons; Joint Section on Neurotrauma and Critical Care, AANS/CNS, Carney NA, et al. Guidelines for the management of severe traumatic brain injury. Introduction. J Neurotrauma 2007; 24 Suppl 1: S1–2. Finfer S, Bellomo R, Boyce N, French J, Myburgh J, Norton R, et al. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med 2004; 350: 2247–256. Stein SC, Fabbri A, Servadei F, Glick HA. A critical comparison of clinical decision instruments for computed tomographic scanning in mild closed traumatic brain injury in adolescents and adults. Ann Emerg Med 2009; 53: 180–188. Melnick ER, Szlezak CM, Bentley SK, Dziura JD, Kotlyar S, Post LA. CT overuse for mild traumatic brain injury. Jt Comm J Qual Patient Saf 2012; 38: 483–489. Eagles D, Stiell IG, Clement CM, Brehaut J, Taljaard M, Kelly AM, et al. International survey of emergency physicians' awareness and use of the Canadian Cervical-Spine Rule and the Canadian Computed Tomography Head Rule. Acad Emerg Med 2008; 15: 1256–1261. Smits M, Dippel DW, Steyerberg EW, de Haan GG, Dekker HM, Vos PE, et al. Predicting intracranial traumatic findings on computed tomography in patients with minor head injury: the CHIP prediction rule. Ann Intern Med 2007; 146: 397–405. Brown CV, Weng J, Oh D, Salim A, Kasotakis G, Demetriades D, et al. Does routine serial computed tomography of the head influence management of traumatic brain injury? A prospective evaluation. J Trauma 2004; 57: 939–943. Sperry JL, Gentilello LM, Minei JP, Diaz-Arrastia RR, Friese RS, Shafi S. Waiting for the patient to "sober up": Effect of alcohol intoxication on glasgow coma scale score of brain injured patients. J Trauma 2006; 61: 1305–1311. Godbout BJ, Lee J, Newman DH, Bodle EE, Shah K. Yield of head CT in the alcohol-intoxicated patient in the emergency department. Emerg Radiol 2011; 18: 381–384. Lee J, Evans CS, Singh N, Kirschner J, Runde D, Newman D, et al. Head computed tomography utilization and intracranial hemorrhage rates. Emerg Radiol 2013; 20: 219–223. Downey DM, Monson B, Butler KL, Fortuna GR Jr, Saxe JM, Dolan JP, et al. Does platelet administration affect mortality in elderly head-injured patients taking antiplatelet medications? Am Surg 2009; 75: 1100–1103. Nishijima DK, Zehtabchi S, Berrong J, Legome E. Utility of platelet transfusion in adult patients with traumatic intracranial hemorrhage and preinjury antiplatelet use: a systematic review. J Trauma Acute Care Surg 2012; 72: 1658–1663. Ivascu FA, Howells GA, Junn FS, Bair HA, Bendick PJ, Janczyk RJ. Rapid warfarin reversal in anticoagulated patients with traumatic intracranial hemorrhage reduces hemorrhage progression and mortality. J Trauma 2005; 59: 1131–1137; discussion 1137–1139. Edwards P, Arango M, Balica L, Cottingham R, El-Sayed H, Farrell B, et al. Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticosteroid in adults with head injury-outcomes at 6 months. Lancet 2005; 365: 1957–1959. Roberts I, Shakur H, Ker K, Coats T; CRASH-2 Trial collaborators. Antifibrinolytic drugs for acute traumatic injury. Cochrane Database Syst Rev 2011; (1): CD004896. Yank V, Tuohy CV, Logan AC, Bravata DM, Staudenmayer K,
World J Emerg Med, Vol 4, No 4, 2013
46
47
48
49
50
51
52
Eisenhut R, et al. Systematic review: benefits and harms of inhospital use of recombinant factor VIIa for off-label indications. Ann Intern Med 2011; 154: 529–540. Diringer MN, Skolnick BE, Mayer SA, Steiner T, Davis SM, Brun NC, et al. Thromboembolic events with recombinant activated factor VII in spontaneous intracerebral hemorrhage: results from the Factor Seven for Acute Hemorrhagic Stroke (FAST) trial. Stroke 2010; 41: 48–53. Schierhout G, Roberts I. WITHDRAWN: Antiepileptic drugs for preventing seizures following acute traumatic brain injury. Cochrane Database Syst Rev 2012; 6: CD000173. Temkin NR, Dikmen SS, Anderson GD, Wilensky AJ, Holmes MD, Cohen W, et al. Valproate therapy for prevention of posttraumatic seizures: a randomized trial. J Neurosurg 1999; 91: 593–600. Chang BS, Lowenstein DH; Quality Standards Subcommittee of the American Academy of Neurology. Practice parameter: antiepileptic drug prophylaxis in severe traumatic brain injury: report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2003; 60: 10–16. Darrah SD, Chuang J, Mohler LM, Chen X, Cummings EE, Burnett T, et al. Dilantin therapy in an experimental model of traumatic brain injury: effects of limited versus daily treatment on neurological and behavioral recovery. J Neurotrauma 2011; 28: 43–55. Pieracci FM, Moore EE, Beauchamp K, Tebockhorst S, Barnett CC, Bensard DD, et al. A cost-minimization analysis of phenytoin versus levetiracetam for early seizure pharmacoprophylaxis after traumatic brain injury. J Trauma Acute Care Surg 2012; 72: 276–281. Coester A, Neumann CR, Schmidt MI. Intensive insulin therapy in severe traumatic brain injury: a randomized trial. J Trauma 2010; 68: 904–911.
259
53 Yang M, Guo Q, Zhang X, Sun S, Wang Y, Zhao L, et al. Intensive insulin therapy on infection rate, days in NICU, inhospital mortality and neurological outcome in severe traumatic brain injury patients: a randomized controlled trial. Int J Nurs Stud 2009; 46: 753–758. 54 Bor-Seng-Shu E, Figueiredo EG, Amorim RL, Teixeira MJ, Valbuza JS, de Oliveira MM, et al. Decompressive craniectomy: a meta-analysis of influences on intracranial pressure and cerebral perfusion pressure in the treatment of traumatic brain injury. J Neurosurg 2012; 117: 589–596. 55 Sahuquillo J, Arikan F. Decompressive craniectomy for the treatment of refractory high intracranial pressure in traumatic brain injury. Cochrane Database Syst Rev 2006; (1): CD003983. 56 Whitmore RG, Thawani JP, Grady MS, Levine JM, Sanborn MR, Stein SC. Is aggressive treatment of traumatic brain injury cost-effective? J Neurosurg 2012; 116: 1106–1113. 57 Timmons SD, Ullman JS, Eisenberg HM. Craniectomy in diffuse traumatic brain injury. N Engl J Med 2011; 365: 373; author reply 376. 58 Harris OA, Colford JM Jr, Good MC, Matz PG. The role of hypothermia in the management of severe brain injury: a metaanalysis. Arch Neurol 2002; 59: 1077–1083. 59 Sydenham E, Roberts I, Alderson P. Hypothermia for traumatic head injury. Cochrane Database Syst Rev 2009; (2): CD001048. 60 Clifton GL, Valadka A, Zygun D, Coffey CS, Drever P, Fourwinds S, et al. Very early hypothermia induction in patients with severe brain injury (the National Acute Brain Injury Study: Hypothermia II): a randomised trial. Lancet Neurol 2011; 10: 131–139.
Received April 15, 2013 Accepted after revision October 11, 2013
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