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Evaluation and Management of Moderate to Severe Pediatric Head Trauma
The Journal of Emergency Medicine, Vol. 37, No. 1, pp. 63– 68, 2009 Copyright © 2009 Elsevier Inc. Printed in the USA. All rights reserved 0736-4679/09 $–see front matter
doi:10.1016/j.jemermed.2009.02.003
Trauma Reports1
EVALUATION AND MANAGEMENT OF MODERATE TO SEVERE PEDIATRIC HEAD TRAUMA Anand Swaminathan,
MD, MPH,*
Phil Levy,
MD,†‡
and Eric Legome,
MD§
*New York University (NYU)/Bellevue Emergency Medicine Residency, Department of Emergency Medicine, NYU Medical Center, New York, New York, †Department of Emergency Medicine, Detroit Receiving Hospital, Detroit, Michigan, ‡Emergency Medicine Residency, Wayne State University School of Medicine, Detroit, Michigan, and §Department of Emergency Medicine, St. Vincent’s Hospital Manhattan, New York, New York Reprint Address: Eric Legome, MD, Department of Emergency Medicine, St. Vincent’s Hospital Manhattan, 103 West 12th Street, New York, NY 10011
e Abstract—A case of pediatric head trauma is presented with a detailed discussion of current concepts in evaluation and treatment. Management of the moderate to severe head-injured child is reviewed, and best practices for emergency department treatment are discussed. Background: Pediatric head trauma is a common and potentially devastating injury. Thorough knowledge of the clinical evaluation and treatment will assist the emergency physician in providing optimal care. Discussion: Using a case-based scenario, the initial management strategies along with rationale evidence-based treatments are reviewed. Conclusions: Computed tomography scan is the diagnostic test of choice for the moderate to severe head-injured pediatric patient. Several unique scales to describe and prognosticate the head injury are discussed, although currently, the Glasgow Coma Scale is still the most commonly accepted one. Similar to the adult patient, avoidance of hypotension and hypoxia are key to decreasing mortality. Etomidate and succinylcholine remain the choice of medications for intubation. Hyperventilation should be avoided. © 2009 Elsevier Inc.
CASE PRESENTATION A 35-day-old ex-premature 35-week boy was brought in by Emergency Medical Services (EMS) after a witnessed fall out of a baby carrier down 15 carpeted steps. The parents stated that the child continued breathing, but was otherwise unresponsive to voice or pain for 30 s, and then began to cry inconsolably. They denied witnessing vomiting or seizure-like activity after the fall. EMS secured the patient in his baby carrier and transported the child to the Emergency Department (ED). En route, the patient was crying, with episodes of decreased responsiveness. On ED arrival, vital signs revealed a blood pressure of 51/24 mm Hg, a heart rate of 171 beats/min, respiratory rate of 44 breaths/min, and an oxygen saturation of 100% on room air. On primary survey, the airway appeared patent. Breathing was normal and breath sounds were equal bilaterally. The child was pink in color with strong brachial and femoral pulses bilaterally. He opened his eyes to painful stimuli but not spontaneously, and would move all four extremities equally without any specific response to pain. The patient made no vocal response. The initial pediatric Glasgow Coma Scale (GCS) was 6. Immediately upon arrival, intravenous access was established, the patient was placed on a monitor, and
e Keywords—pediatric head trauma; resuscitation; TBI; pediatric critical care
1
Trauma Reports of NYU/Bellevue Emergency Medicine Residency, New York, NY.
RECEIVED: 24 September 2008; FINAL ACCEPTED: 5 February 2009
SUBMISSION RECEIVED:
30 January 2009;
63
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A. Swaminathan et al.
blow-by oxygen was delivered. The patient’s neck was also immobilized. Secondary survey revealed a large hematoma over the left frontoparietal region without any evidence of laceration. The anterior fontanelle was open and flat and there were no palpable skull fractures. Pupils were 5 mm bilaterally and reactive to light. The chest, abdomen, and extremity examinations were unremarkable. A bedside FAST (focused assessment with sonography in trauma) examination revealed no evidence of free intra-peritoneal fluid or pericardial effusion. After the secondary survey was completed, the patient had recurrent, intermittent apneic episodes lasting 5– 6 s each. Bag-valve-mask ventilation was initiated and intubation was attempted. Intubation was complicated by emesis and desaturation, but eventually the airway was secured. Because the blood pressure after intubation was 45/23 mm Hg, a 60-cc bolus of normal saline was administered, with a resultant increase in blood pressure to 57/35 mm Hg.
BACKGROUND Roughly 650,000 children each year in the United States are evaluated in the ED for head trauma, 80% of which are considered minor events. Despite this, head trauma remains the principal cause of trauma-related morbidity and mortality in the pediatric population. The degree of head trauma is defined by the presenting GCS, where a score of 14 –15 is defined as mild (occasionally 13 is included in mild), 9 –13 as moderate, and 3– 8 as severe. Although falls exist as the primary etiology of head trauma in children ⬍ 2 years of age, abuse stands as the leading cause of severe cranial injury. The overall mortality rate of isolated severe pediatric head injury is 6 –10%, which is significantly better than the 30 –50% mortality rates in similarly injured adults (1). In addition, 70% of patients that present with GCS scores of 3 or 4 have good neurologic recovery and 95% of severe pediatric head trauma patients over the age of 5 years were able to return to the appropriate grade level (1). The pathophysiology of pediatric head injury, however, differs substantially from that of adult head injury. Open cranial sutures result in increased susceptibility to injury from blunt forces and delay the onset of herniation as they allow for a greater amount of intracranial expansion. Pediatric brains are also less myelinated than adults, predisposing them to shearing forces (2,3). The effects of hypoxia, hypotension, and intracranial hypertension on neurologic outcome are more profound in pediatric head trauma patients, primarily due to the development of secondary brain injury. Secondary brain injury is the delayed cellular damage and dysfunction,
Table 1. Major Causes of Secondary Brain Injury Hypoxia Hyperthermia Intracranial hypertension Anemia Vasospasm Compression from mass effect
Hypotension Hyperglycemia/hypoglycemia Hypocapnia/hypercapnia Cerebral edema Seizures
which develops subsequent to the initial or primary insult and is influenced by both intracranial and systemic factors. As such, there is potential to decrease or ameliorate its intensity, duration, and ultimate effect on outcome through early, aggressive, comprehensive patient care. Table 1 comprises the major causes of secondary injury.
DISCUSSION OF INITIAL MANAGEMENT An expedited assessment of airway and breathing is essential. Hypoxia is a leading cause of secondary neuronal injury and must be promptly reversed. The presence of hypoxia has been associated with a two- to fourfold increase in poor outcomes, as defined by death, severe disability, or persistent vegetative state (4). Early airway management ensures oxygenation and decreases the risk of respiratory compromise due to secondary cerebral edema affecting the respiratory center. The decision to intubate the head-injured patient is a clinical one, with mental status serving as the primary factor of importance. For adults, a GCS ⱕ 8 in the setting of head trauma is commonly considered an absolute indication to initiate rapid establishment of a definitive airway; because the GCS relies on verbal responses, such a rule can be difficult to apply to young children. A pediatric GCS with modified verbal response scores exists as a substitute but is still of limited utility in infants (Table 2). The infant face scale (IFS) (Table 3) was developed to address this deficiency and serves as a useful adjunct in the evaluation of head-injured young patients (5). Despite its potential, the IFS is not widely used to guide the management of pediatric traumatic brain injury (TBI) because its use has not been standardized in infants and children. In addition, unlike in adults, there is no widely accepted IFS score that indicates the need for intubation. Thus, most pediatric literature continues to base recommendations on GCS scores. Because severe agitation can interfere with stabilization and patient management, many advocate early intubation for these patients as well. Rapid sequence intubation (RSI) with sedation and paralysis is the preferred technique for airway management in patients with suspected TBI. Based on the belief that children have a more pronounced vagal response to intubation, pre-medication with atropine before administra-
Evaluation and Management of Pediatric Head Trauma
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Table 2. Pediatric Glasgow Coma Score (GCS) Assessed Response Best eye response Spontaneously To verbal stimulation or to touch To pain No response Best verbal response Smiles, oriented to sounds, follows objects, interacts Cries but is consolable, inappropriate interactions Inconsistently consolable, moaning Inconsolable, agitated No vocal response Motor Normal spontaneous movement Withdraws to touch Withdraws to pain Flexion abnormal Extension, either spontaneous or to painful stimuli Flaccid
Score 4 3 2 1 5 4 3 2 1 6 5 4 3 2 1
tion of sedative and paralytic agents has been advocated for the pediatric population (6 – 8). Recent literature, however, has demonstrated equivalence in the incidence of vagally mediated bradycardia during laryngoscopy and intubation in pediatric patients who were pre-medicated with atropine vs. those that were not, regardless of the paralytic agent used (9,10). Although there is minimal downside to the use of atropine before intubation, it does cause mydriasis, which can last for hours. This effect removes the clinician’s ability to diagnose brain herniation based on pupillary response and may delay emergency decompressive measures. Intravenous lidocaine use has also been advocated before initiation of RSI, largely based on the theoretical ability of this medication to blunt the transient rise in intracranial pressure (ICP) that occurs with laryngeal instrumentation. However, there is a lack of evidence supporting either reduction in ICP or improvement in neurological outcome with lidocaine use before RSI (11). Because pretreatment strategies require time to achieve desired effect, they may delay the interval to definitive airway control. Therefore, they should be utilized, if at all, only when airway compromise is not imminent. Once a decision has been made to perform RSI, choice of sedative agent is important. Medications such as thiopental, propofol, and midazolam should be used cautiously due to their propensity to cause hypotension and thus lower cerebral perfusion pressure (12). The ideal agent is one that does not compromise the patients’ hemodynamic parameters. The use of ketamine for induction has been discouraged due to the belief that it increased ICP, cerebral oxygen consumption, and cerebral metabolism, primarily via inhibitory effect on catecholamine reuptake. However, more recent, although not
definitive, studies argue against the detrimental effects on ICP (13–15). In addition, ketamine maintains mean arterial pressure, thus avoiding hypotension during RSI. Etomidate is a rapid-acting, short-duration sedative with minimal hemodynamic effects. Etomidate is also thought to exert neuroprotective effects through a decrease in ICP and a reduction in the metabolic rate and oxygen consumption of the brain, making it an ideal agent for use in TBI (16,17). Succinylcholine has been used as the paralytic agent of choice for RSI in both adults and children. The onset of succinycholine is approximately 45 s, and the duration of action is 3–5 min. Because it is a depolarizing paralytic agent, succinylcholine may elevate ICP transiently, but there is no clinical evidence of an associated increase in morbidity or mortality related to its use (18,19). Nondepolarizing paralytic agents such as rocuronium may be substituted to avoid the potential for increased ICP, but they have a delayed onset of action and prolonged paralysis in comparison to succinycholine. Higher doses of rocuronium (1.2 mg/kg) have been shown to yield comparable onset times to succinylcholine, but a recent Cochrane review concluded that succinylcholine was superior due to its shorter duration of action (20,21). Pretreatment with a defasciculating dose (1/10th of the standard dose) of a non-depolarizing agent before administration of succinycholine may diminish the development of fasciculations (which are thought to be respon-
Table 3. Infant Face Scale (IFS) Assessed Response Eye opening Spontaneously To verbal stimulation or to touch To pain No response Verbal/facial response Cries (grimaces with crying sounds or tears) spontaneously, with handling, or to minor pain; alternating with periods of quiet wakefulness when not asleep Cries (grimaces with crying sounds or tears) spontaneously, with handling, or to minor pain; alternating with sleep only (no quiet wakefulness maintained) Cries to deep pain only Grimaces only to pain (facial movement without sounds or tears) No facial expression to pain Motor Spontaneous normal movements Spontaneous normal movements reduced in frequency or excursion; hypoactive Non-specific movement to deep pain only Abnormal rhythmic spontaneous movements; seizure-like activity Extension, either spontaneous or to painful stimuli Flaccid
Score 4 3 2 1 5
4
3 2 1 5 5 4 3 2 1
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sible for the increase in ICP) but to date, no studies have demonstrated the efficacy of this and it is not routinely recommended (22). In the past, aggressive hyperventilation was commonly performed in an effort to reduce ICP in those with TBI (23). This was based on the assumption that brain hyperemia was common after TBI and that hyperventilation would restore blood pressure autoregulation through induced hypocapnia, thereby improving cerebral metabolism and selectively increasing perfusion to ischemic areas. Hyperventilation is known, however, to cause cerebral vasoconstriction with an associated decrease in cerebral blood flow. Although early studies reported a clinical benefit from hyperventilation, more recent data show an association with worsened neurological outcomes, that is, greater likelihood of moderate to severe disability (24 –26). This is thought to be related to a combination of hyperventilation-induced ischemia in both injured and intact parts of the brain secondary to decreasing cerebral blood flow and a depletion of bicarbonate in the brain with resultant impairment in buffering capacity. As such, current recommendations are for ventilation to be titrated to eucapnea, with reservation of hyperventilation solely for TBI patients who demonstrate signs of impending cerebral herniation. Children with moderate to severe head injury are also at risk for associated cervical spine injuries. During intubation, therefore, in-line cervical spine immobilization must be maintained to prevent further injury. The prevalence of cervical spine injury in adult severe blunt head injury is estimated to be 6 – 8% (27,28). Pediatric spinal cord injuries are much less common than in adults, accounting for only 0.3–10% of all spinal cord injuries (29). Sixty to eighty percent of all spinal cord injuries in patients ⬍ 8 years of age occur in the cervical spine due to the relatively larger head and underdeveloped neck muscles (only 30 – 40% of spinal cord injuries in adults are in the cervical spine) (30). Once the airway has been secured and ventilation established, the patient’s circulatory status must be addressed. Hypotension is the most influential secondary brain insult determining short-term mortality, with a threefold increase (61% vs. 22%) after the occurrence of a single episode (31,32). Although hypotension is defined in the pediatric literature as a systolic blood pressure measurement below the fifth percentile of normal for age, Vavilala et al. demonstrated an increase in mortality for TBI patients when systolic blood pressure drops below the 75th percentile (33). Although isolated head trauma can cause hypotension in children, alternative sources such as blood loss from other injuries should be sought. Prompt fluid resuscitation with normal saline should be initiated immediately to avoid hypotension. Although some research has found that children suffer-
A. Swaminathan et al.
ing TBI with elevated systolic blood pressures had higher survival rates, there is currently no role for inducing supranormal blood pressure (34). FURTHER MANAGEMENT IN THE EMERGENCY DEPARTMENT Before diagnostic imaging, the patient had a generalized tonic-clonic seizure. Phenobarbital was administered, with cessation of seizure activity. The patient was then transported to Radiology, where computed tomography (CT) scanning of the head, cervical spine, chest, abdomen, and pelvis were obtained. Non-contrast head CT (NCHCT) revealed multiple intracranial injuries, including left anterior and posterior subgaleal hematomas, a minimally displaced left parietal bone fracture, left epidural vs. subdural hematoma, right frontal subdural hematoma, multiple areas of subarachnoid hemorrhage, right temporal horn hemorrhagic contusion, and a left lateral ventricle interventricular hemorrhage, but no evidence of midline shift or mass effect (Figure 1). Cervical spine CT scan demonstrated no fractures, and CT scans of the chest, abdomen, and pelvis showed no injuries. On return to the ED, the patient was loaded with intravenous phenytoin for further seizure prophylaxis. OTHER ACUTE INTERVENTIONS Pediatric critical care consensus statements recommend aggressive ICP-directed therapy in all children with se-
Figure 1. Non-contrast head computed tomography scan of the patient. Thick arrow: subarachnoid hemorrhage; thin arrow: subdural hemorrhage; triangle: intraventricular blood.
Evaluation and Management of Pediatric Head Trauma
vere TBI and a GCS score ⬍ 8 (35). The literature supporting these recommendations is comprised of a number of small, single-center, observational and retrospective studies. No randomized controlled trial has been performed in any age group evaluating the effect of ICP monitoring on long-term neurologic outcomes. Intracranial hypertension is a major predictor of poor neurologic outcome and increased mortality but can be controlled with medical interventions (hyperosmolar and hyperventilation therapy) as well as surgical interventions (cerebral spinal fluid drainage and decompressive craniotomy). A discussion of these interventions is beyond the scope of this review, but it is important to appropriately identify those patients, using historical and clinical factors combined with imaging, who may require early neurosurgical intervention and aggressive ongoing management. Clinical accuracy for this, however, is limited. Open fontanels and sutures do not prevent the development of increased ICP or diminish the utility of ICP monitoring (36). Studies demonstrate that up to 86% of children with an initial GCS ⱕ 8 had ICP measurements ⬎ 20 mm Hg (37). In addition, 53– 63% of patients with severe TBI in combination with abnormal NCHCT had elevated ICP (38). A normal admission NCHCT does not rule out increased ICP (39). Non-surgical management of pediatric patients with confirmed or suspected increases in ICP can be challenging. Prophylactic use of hyperosmolar therapy (mannitol or hypertonic saline) in children with severe TBI is not advocated. Current recommendations are to use these agents only in conjunction with an ICP monitor and documented elevation in ICP (40,41). However, mannitol may be given empirically for signs and symptoms of herniation or impending herniation. This includes acute decline in mental status and unilateral dilatated and unresponsive pupil. Prophylactic anti-seizure medication is appropriate to initiate, and use of these agents should be continued for 7 days in all patients with moderate to severe head trauma defined as an initial GCS ⱕ 8 (42). No one agent has been clearly proven superior. Up to 40% of these patients will experience early posttraumatic seizures (43). The risk of seizure development increases threefold in children under the age of 2 years (vs. those older than the age of 12) (44). Seizures can cause secondary brain injury by a number of different mechanisms, including hypoxia, hypercarbia, and increased cerebral metabolic demand, and will cause further increases in ICP. Multiple studies have demonstrated reduction in the incidence of early post-traumatic seizures with the use of anti-seizure medications, but there are no well-designed studies to suggest a preferred or superior agent (42,45). It is important to remember however, that early seizure prophylaxis does not affect
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the risk of developing late post-traumatic (⬎ 7 days after event) seizures (46).
DISCUSSION The management of pediatric head trauma in the ED focuses on rapid stabilization, diagnosis, and attempts to reduce the development of secondary brain injury. Appropriate interventions can have a significant effect on neurologic outcome. Hypoxia and hypotension must be avoided or rapidly corrected due to the association of each with extremely poor outcomes. Early definitive airway control should be considered in all patients both to avoid hypoxia and facilitate further management. Hyperventilation should be avoided unless signs of herniation are present, as it has been shown to increase cerebral ischemia. Early seizure prophylaxis should be initiated in all patients with severe TBI. Finally, because many of the necessary therapeutic modalities rely on invasive monitoring, close cooperation between the emergency physician and neurosurgeon is necessary.
CONCLUSION The patient was evaluated by the neurosurgical service and it was determined that acute invasive surgical intervention was not indicated, as there was not an easily identifiable lesion causing mass effect that would be amenable to operative removal. The patient was admitted to the Pediatric Intensive Care Unit and repeat NCHCT demonstrated no change in the injury patterns previously described. On hospital day 3, the patient was successfully extubated and enteral feeds were started. Repeat NCHCT on hospital day 6 showed evidence of resolving subdural and intraventricular hemorrhage. The patient was discharged home on hospital day 7 on a phenobarbital taper. At the time, the patient showed appropriate neurological development for his age. Due to the patient’s young age, the potential for long-term neurologic sequelae remained uncertain upon discharge.
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68 5. Berger RP, Adelson PD. Evaluation and management of pediatric head trauma in the emergency department: current concepts and state-of-the-art research. Clin Pediatr Emerg Med 2005;6:8 –15. 6. Yamamoto LG, Yim GK, Britten AG. Rapid sequence anesthesia induction for emergency intubation. Pediatr Emerg Care 1990;6: 200 –13. 7. Tobias JD. Airway management for pediatric emergencies. Pediatr Ann 1996;25:317–28. 8. McAllister JD, Gnauck KA. Rapid sequence intubation of the pediatric patient. Pediatr Clin North Am 1999;46:1249 – 84. 9. Fastle RK, Roback MG. Pediatric rapid sequence intubation: incidence of re-flex bradycardia and effects of pretreatment with atropine. Pediatr Emerg Care 2004;20:651–5. 10. Bean A, Jones J. Atropine: re-evaluating its use during paediatric RSI. Emerg Med J 2007;24:361–2. 11. Robinson N, Clancy M. In patients with head injury undergoing rapid sequence intubation, does pretreatment with intravenous lignocaine/lidocaine lead to an improved neurological outcome? A review of the literature. Emerg Med J 2001;18:453–7. 12. Zelicof-Paul A, Smith-Lockridge A, Schnadower D, et al. Controversies in rapid sequence intubation in children. Curr Opin Pediatr 2005;17:355– 62. 13. Bourgoin A, Albanese J, Wereszczynski N, et al. Safety of sedation with ketamine in severe head injury patients: comparison with sufentanil. Crit Care Med 2003;31:711–7. 14. Bourgoin A, Albanese J, Leone M, Sampol-Manos E, Viiand X, Martin C. Effects of sufentanil or ketamine administered in targetcontrolled infusion on the cerebral hemodynamics of severely brain-inured patients. Crit Care Med 2005;33:1109 –13. 15. Himmelesher S, Durieux ME. Revising a dogma: ketamine for patients with neurological injury? Anesth Analg 2005;101:524 –34. 16. Bergen JM, Smith DC. A review of etomidate for rapid sequence intubation in the emergency department. J Emerg Med 1997;15: 221–30. 17. Modica PA, Tempelhoff R. Intracranial pressure during induction of anaesthesia and tracheal intubation with etomidate-induced EEG burst suppression. Can J Anesth 1992;39:36 – 41. 18. Brown MM, Parr MJ, Manara AR. The effect of suxamethonium on intracranial pressure and cerebral perfusion in patients with severe head injuries following blunt trauma. Eur J Anaesth 1996; 13:474 –77. 19. Kovarik WD, Mayberg TS, Lam AM, et al. Succinylcholine does not change intracranial pressure, cerebral blood flow velocity, or the electroencephalogram in patients with neurologic injury. Anesth Analg 1994;78:469 –73. 20. Verma RK, Goordayal R, Jaiswal S, Sinha GK. A comparative study of the intubating conditions and cardiovascular effects following succinylcholine and rocuronium in adult elective surgical patients. Internet J Anesthesiol 2007;14(1). 21. Perry JJ, Lee JS, Sillberg VAH, Wells GA. Rocuronium versus succinylcholine for rapid sequence induction intubation. Cochrane Database Syst Rev 2007;(3):CD002788. 22. 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; 18:373–5. 23. Bruce D, Raphaely R, Goldberg A, et al. Pathophysiology, treatment and outcome following severe head injury in children. Childs Brain 1979;5:174 –9. 24. Muizelaar JP, Marmarou A, Ward JD, et al. Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. J Neurosurg 1991;75:731–9. 25. Skippen P, Seear M, Poskitt K, et al. Effect of hyperventilation on regional cerebral blood flow in head-injured children. Crit Care Med 1997;25:1402–9. 26. Stringer WA, Hasso AN, Thompson JR, Hinshaw DB, Jordan KG. Hyperventilation-induced cerebral ischemia in patients with acute brain lesions: demonstration by Xenon-enhanced CT. AJNR Am J Neuroradiol 1993;14:475– 84.
A. Swaminathan et al. 27. Hills MW, Deane SA. Head injury and facial injury: is there an increased risk of cervical spine injury? J Trauma 1993;34:549 –54. 28. Michael DB, Guyot DR, Darmody WR. Coincidence of head and cervical spine injury. J Neurotrauma 1989;6:177– 89. 29. Dias MS. Traumatic brain and spinal cord injury. Pediatr Clin North Am 2004;51:271–303. 30. Cirak B, Ziegfeld S, Knight VM, Chang D, Avellino AM, Paidas CN. Spinal injuries in children. J Pediatr Surg 2004;39:607–12. 31. Adelson PD, Bratton SL, Carney NA, et al. Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents. Chapter 4. Resuscitation of blood pressure and oxygenation and pre-hospital brain-specific therapies for the severe pediatric traumatic brain injury patient. Pediatr Crit Care Med 2003;S12– 8. 32. Pigula FA, Wald SL, Shackford SR, et al. The effect of hypotension and hypoxia on children with severe head injuries. J Pediatr Surg 1993;28:310 – 4. 33. Vavilala MS, Bowen A, Lam AM, et al. Blood pressure and outcome after severe pediatric traumatic brain injury. J Trauma 2003;55:1039 – 44. 34. White JR, Farukhi Z, Bull C, et al. Predictors of outcome in severely head-injured children. Crit Care Med 2001;29:534 –50. 35. Adelson PD, Bratton SL, Carney NA, et al. Guidelines for the acute medical management of severe traumatic brain injury in infants, children and adolescents. Chapter 5. Indications for intracranial pressure monitoring in pediatric patients with severe traumatic brain injury. Pediatr Crit Care Med 2003;4(3 Suppl):S19 –24. 36. Cho DY, Wang YC, Chi CS. Decompressive craniotomy for acute shaken/impact syndrome. Pediatr Neurosurg 1995;23:192– 8. 37. Shapiro K, Marmarou A. Clinical applications of the pressurevolume index in treatment of pediatric head injuries. J Neurosurg 1982;56:819 –25. 38. Narayan RK, Kishore PR, Becker DP, et al. Intracranial pressure: to monitor or not to monitor? A review of our experience with severe head injury. J Neurosurg 1982;56:650 –9. 39. O’Sullivan MG, Statham PF, Jones PA, et al. Role of intracranial pressure monitoring in severely head injured patients without signs of intracranial hypertension on initial CT. J Neurosurg 1994;80: 46 –50. 40. Adelson PD, Bratton SL, Carney NA, et al. Guidelines for the acute medical management of severe traumatic brain injury in infants, children and adolescents. Chapter 11. Use of hyperosmolar therapy in the management of severe pediatric traumatic brain injury. Pediatr Crit Care Med 2003;4(3 Suppl):S40 – 4. 41. Qureshi AI, Geocadin RG, Suarez JI, Ulatowski JA. Long-term outcome after medical reversal of transtentorial herniation in patients with supratentorial mass lesions. Crit Care Med 2000;28: 1556 – 64. 42. Lewis RJ, Yee L, Inkelis SH, et al. Clinical predictors of posttraumatic seizures in children with head trauma. Ann Emerg Med 1993;22:1114 – 8. 43. Adelson PD, Bratton SL, Carney NA, et al. Guidelines for the acute medical management of severe traumatic brain injury in infants, children and adolescents. Chapter 12. Use of hyperventilation in the acute management of severe pediatric traumatic brain injury. Pediatr Crit Care Med 2003;4(3 Suppl):S45– 8. 44. Ratan SK, Kulshreshtha R, Pandey RM. Predictors of posttraumatic convulsions in head-injured children. Pediatr Neurosurg 1999;30:127–31. 45. Tilford JM, Simpson PM, Yeh TS, et al. Variation in therapy and outcome for pediatric head trauma patients. Crit Care Med 2001; 29:1056 – 61. 46. Adelson PD, Bratton SL, Carney NA, et al. Guidelines for the acute medical management of severe traumatic brain injury in infants, children and adolescents. Chapter 19. The role of antiseizure prophylaxis following severe pediatric traumatic brain injury. Pediatr Crit Care Med 2003;4(3 Suppl):S72–5.
doi:10.1016/j.jemermed.2009.02.003
Trauma Reports1
EVALUATION AND MANAGEMENT OF MODERATE TO SEVERE PEDIATRIC HEAD TRAUMA Anand Swaminathan,
MD, MPH,*
Phil Levy,
MD,†‡
and Eric Legome,
MD§
*New York University (NYU)/Bellevue Emergency Medicine Residency, Department of Emergency Medicine, NYU Medical Center, New York, New York, †Department of Emergency Medicine, Detroit Receiving Hospital, Detroit, Michigan, ‡Emergency Medicine Residency, Wayne State University School of Medicine, Detroit, Michigan, and §Department of Emergency Medicine, St. Vincent’s Hospital Manhattan, New York, New York Reprint Address: Eric Legome, MD, Department of Emergency Medicine, St. Vincent’s Hospital Manhattan, 103 West 12th Street, New York, NY 10011
e Abstract—A case of pediatric head trauma is presented with a detailed discussion of current concepts in evaluation and treatment. Management of the moderate to severe head-injured child is reviewed, and best practices for emergency department treatment are discussed. Background: Pediatric head trauma is a common and potentially devastating injury. Thorough knowledge of the clinical evaluation and treatment will assist the emergency physician in providing optimal care. Discussion: Using a case-based scenario, the initial management strategies along with rationale evidence-based treatments are reviewed. Conclusions: Computed tomography scan is the diagnostic test of choice for the moderate to severe head-injured pediatric patient. Several unique scales to describe and prognosticate the head injury are discussed, although currently, the Glasgow Coma Scale is still the most commonly accepted one. Similar to the adult patient, avoidance of hypotension and hypoxia are key to decreasing mortality. Etomidate and succinylcholine remain the choice of medications for intubation. Hyperventilation should be avoided. © 2009 Elsevier Inc.
CASE PRESENTATION A 35-day-old ex-premature 35-week boy was brought in by Emergency Medical Services (EMS) after a witnessed fall out of a baby carrier down 15 carpeted steps. The parents stated that the child continued breathing, but was otherwise unresponsive to voice or pain for 30 s, and then began to cry inconsolably. They denied witnessing vomiting or seizure-like activity after the fall. EMS secured the patient in his baby carrier and transported the child to the Emergency Department (ED). En route, the patient was crying, with episodes of decreased responsiveness. On ED arrival, vital signs revealed a blood pressure of 51/24 mm Hg, a heart rate of 171 beats/min, respiratory rate of 44 breaths/min, and an oxygen saturation of 100% on room air. On primary survey, the airway appeared patent. Breathing was normal and breath sounds were equal bilaterally. The child was pink in color with strong brachial and femoral pulses bilaterally. He opened his eyes to painful stimuli but not spontaneously, and would move all four extremities equally without any specific response to pain. The patient made no vocal response. The initial pediatric Glasgow Coma Scale (GCS) was 6. Immediately upon arrival, intravenous access was established, the patient was placed on a monitor, and
e Keywords—pediatric head trauma; resuscitation; TBI; pediatric critical care
1
Trauma Reports of NYU/Bellevue Emergency Medicine Residency, New York, NY.
RECEIVED: 24 September 2008; FINAL ACCEPTED: 5 February 2009
SUBMISSION RECEIVED:
30 January 2009;
63
64
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blow-by oxygen was delivered. The patient’s neck was also immobilized. Secondary survey revealed a large hematoma over the left frontoparietal region without any evidence of laceration. The anterior fontanelle was open and flat and there were no palpable skull fractures. Pupils were 5 mm bilaterally and reactive to light. The chest, abdomen, and extremity examinations were unremarkable. A bedside FAST (focused assessment with sonography in trauma) examination revealed no evidence of free intra-peritoneal fluid or pericardial effusion. After the secondary survey was completed, the patient had recurrent, intermittent apneic episodes lasting 5– 6 s each. Bag-valve-mask ventilation was initiated and intubation was attempted. Intubation was complicated by emesis and desaturation, but eventually the airway was secured. Because the blood pressure after intubation was 45/23 mm Hg, a 60-cc bolus of normal saline was administered, with a resultant increase in blood pressure to 57/35 mm Hg.
BACKGROUND Roughly 650,000 children each year in the United States are evaluated in the ED for head trauma, 80% of which are considered minor events. Despite this, head trauma remains the principal cause of trauma-related morbidity and mortality in the pediatric population. The degree of head trauma is defined by the presenting GCS, where a score of 14 –15 is defined as mild (occasionally 13 is included in mild), 9 –13 as moderate, and 3– 8 as severe. Although falls exist as the primary etiology of head trauma in children ⬍ 2 years of age, abuse stands as the leading cause of severe cranial injury. The overall mortality rate of isolated severe pediatric head injury is 6 –10%, which is significantly better than the 30 –50% mortality rates in similarly injured adults (1). In addition, 70% of patients that present with GCS scores of 3 or 4 have good neurologic recovery and 95% of severe pediatric head trauma patients over the age of 5 years were able to return to the appropriate grade level (1). The pathophysiology of pediatric head injury, however, differs substantially from that of adult head injury. Open cranial sutures result in increased susceptibility to injury from blunt forces and delay the onset of herniation as they allow for a greater amount of intracranial expansion. Pediatric brains are also less myelinated than adults, predisposing them to shearing forces (2,3). The effects of hypoxia, hypotension, and intracranial hypertension on neurologic outcome are more profound in pediatric head trauma patients, primarily due to the development of secondary brain injury. Secondary brain injury is the delayed cellular damage and dysfunction,
Table 1. Major Causes of Secondary Brain Injury Hypoxia Hyperthermia Intracranial hypertension Anemia Vasospasm Compression from mass effect
Hypotension Hyperglycemia/hypoglycemia Hypocapnia/hypercapnia Cerebral edema Seizures
which develops subsequent to the initial or primary insult and is influenced by both intracranial and systemic factors. As such, there is potential to decrease or ameliorate its intensity, duration, and ultimate effect on outcome through early, aggressive, comprehensive patient care. Table 1 comprises the major causes of secondary injury.
DISCUSSION OF INITIAL MANAGEMENT An expedited assessment of airway and breathing is essential. Hypoxia is a leading cause of secondary neuronal injury and must be promptly reversed. The presence of hypoxia has been associated with a two- to fourfold increase in poor outcomes, as defined by death, severe disability, or persistent vegetative state (4). Early airway management ensures oxygenation and decreases the risk of respiratory compromise due to secondary cerebral edema affecting the respiratory center. The decision to intubate the head-injured patient is a clinical one, with mental status serving as the primary factor of importance. For adults, a GCS ⱕ 8 in the setting of head trauma is commonly considered an absolute indication to initiate rapid establishment of a definitive airway; because the GCS relies on verbal responses, such a rule can be difficult to apply to young children. A pediatric GCS with modified verbal response scores exists as a substitute but is still of limited utility in infants (Table 2). The infant face scale (IFS) (Table 3) was developed to address this deficiency and serves as a useful adjunct in the evaluation of head-injured young patients (5). Despite its potential, the IFS is not widely used to guide the management of pediatric traumatic brain injury (TBI) because its use has not been standardized in infants and children. In addition, unlike in adults, there is no widely accepted IFS score that indicates the need for intubation. Thus, most pediatric literature continues to base recommendations on GCS scores. Because severe agitation can interfere with stabilization and patient management, many advocate early intubation for these patients as well. Rapid sequence intubation (RSI) with sedation and paralysis is the preferred technique for airway management in patients with suspected TBI. Based on the belief that children have a more pronounced vagal response to intubation, pre-medication with atropine before administra-
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Table 2. Pediatric Glasgow Coma Score (GCS) Assessed Response Best eye response Spontaneously To verbal stimulation or to touch To pain No response Best verbal response Smiles, oriented to sounds, follows objects, interacts Cries but is consolable, inappropriate interactions Inconsistently consolable, moaning Inconsolable, agitated No vocal response Motor Normal spontaneous movement Withdraws to touch Withdraws to pain Flexion abnormal Extension, either spontaneous or to painful stimuli Flaccid
Score 4 3 2 1 5 4 3 2 1 6 5 4 3 2 1
tion of sedative and paralytic agents has been advocated for the pediatric population (6 – 8). Recent literature, however, has demonstrated equivalence in the incidence of vagally mediated bradycardia during laryngoscopy and intubation in pediatric patients who were pre-medicated with atropine vs. those that were not, regardless of the paralytic agent used (9,10). Although there is minimal downside to the use of atropine before intubation, it does cause mydriasis, which can last for hours. This effect removes the clinician’s ability to diagnose brain herniation based on pupillary response and may delay emergency decompressive measures. Intravenous lidocaine use has also been advocated before initiation of RSI, largely based on the theoretical ability of this medication to blunt the transient rise in intracranial pressure (ICP) that occurs with laryngeal instrumentation. However, there is a lack of evidence supporting either reduction in ICP or improvement in neurological outcome with lidocaine use before RSI (11). Because pretreatment strategies require time to achieve desired effect, they may delay the interval to definitive airway control. Therefore, they should be utilized, if at all, only when airway compromise is not imminent. Once a decision has been made to perform RSI, choice of sedative agent is important. Medications such as thiopental, propofol, and midazolam should be used cautiously due to their propensity to cause hypotension and thus lower cerebral perfusion pressure (12). The ideal agent is one that does not compromise the patients’ hemodynamic parameters. The use of ketamine for induction has been discouraged due to the belief that it increased ICP, cerebral oxygen consumption, and cerebral metabolism, primarily via inhibitory effect on catecholamine reuptake. However, more recent, although not
definitive, studies argue against the detrimental effects on ICP (13–15). In addition, ketamine maintains mean arterial pressure, thus avoiding hypotension during RSI. Etomidate is a rapid-acting, short-duration sedative with minimal hemodynamic effects. Etomidate is also thought to exert neuroprotective effects through a decrease in ICP and a reduction in the metabolic rate and oxygen consumption of the brain, making it an ideal agent for use in TBI (16,17). Succinylcholine has been used as the paralytic agent of choice for RSI in both adults and children. The onset of succinycholine is approximately 45 s, and the duration of action is 3–5 min. Because it is a depolarizing paralytic agent, succinylcholine may elevate ICP transiently, but there is no clinical evidence of an associated increase in morbidity or mortality related to its use (18,19). Nondepolarizing paralytic agents such as rocuronium may be substituted to avoid the potential for increased ICP, but they have a delayed onset of action and prolonged paralysis in comparison to succinycholine. Higher doses of rocuronium (1.2 mg/kg) have been shown to yield comparable onset times to succinylcholine, but a recent Cochrane review concluded that succinylcholine was superior due to its shorter duration of action (20,21). Pretreatment with a defasciculating dose (1/10th of the standard dose) of a non-depolarizing agent before administration of succinycholine may diminish the development of fasciculations (which are thought to be respon-
Table 3. Infant Face Scale (IFS) Assessed Response Eye opening Spontaneously To verbal stimulation or to touch To pain No response Verbal/facial response Cries (grimaces with crying sounds or tears) spontaneously, with handling, or to minor pain; alternating with periods of quiet wakefulness when not asleep Cries (grimaces with crying sounds or tears) spontaneously, with handling, or to minor pain; alternating with sleep only (no quiet wakefulness maintained) Cries to deep pain only Grimaces only to pain (facial movement without sounds or tears) No facial expression to pain Motor Spontaneous normal movements Spontaneous normal movements reduced in frequency or excursion; hypoactive Non-specific movement to deep pain only Abnormal rhythmic spontaneous movements; seizure-like activity Extension, either spontaneous or to painful stimuli Flaccid
Score 4 3 2 1 5
4
3 2 1 5 5 4 3 2 1
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sible for the increase in ICP) but to date, no studies have demonstrated the efficacy of this and it is not routinely recommended (22). In the past, aggressive hyperventilation was commonly performed in an effort to reduce ICP in those with TBI (23). This was based on the assumption that brain hyperemia was common after TBI and that hyperventilation would restore blood pressure autoregulation through induced hypocapnia, thereby improving cerebral metabolism and selectively increasing perfusion to ischemic areas. Hyperventilation is known, however, to cause cerebral vasoconstriction with an associated decrease in cerebral blood flow. Although early studies reported a clinical benefit from hyperventilation, more recent data show an association with worsened neurological outcomes, that is, greater likelihood of moderate to severe disability (24 –26). This is thought to be related to a combination of hyperventilation-induced ischemia in both injured and intact parts of the brain secondary to decreasing cerebral blood flow and a depletion of bicarbonate in the brain with resultant impairment in buffering capacity. As such, current recommendations are for ventilation to be titrated to eucapnea, with reservation of hyperventilation solely for TBI patients who demonstrate signs of impending cerebral herniation. Children with moderate to severe head injury are also at risk for associated cervical spine injuries. During intubation, therefore, in-line cervical spine immobilization must be maintained to prevent further injury. The prevalence of cervical spine injury in adult severe blunt head injury is estimated to be 6 – 8% (27,28). Pediatric spinal cord injuries are much less common than in adults, accounting for only 0.3–10% of all spinal cord injuries (29). Sixty to eighty percent of all spinal cord injuries in patients ⬍ 8 years of age occur in the cervical spine due to the relatively larger head and underdeveloped neck muscles (only 30 – 40% of spinal cord injuries in adults are in the cervical spine) (30). Once the airway has been secured and ventilation established, the patient’s circulatory status must be addressed. Hypotension is the most influential secondary brain insult determining short-term mortality, with a threefold increase (61% vs. 22%) after the occurrence of a single episode (31,32). Although hypotension is defined in the pediatric literature as a systolic blood pressure measurement below the fifth percentile of normal for age, Vavilala et al. demonstrated an increase in mortality for TBI patients when systolic blood pressure drops below the 75th percentile (33). Although isolated head trauma can cause hypotension in children, alternative sources such as blood loss from other injuries should be sought. Prompt fluid resuscitation with normal saline should be initiated immediately to avoid hypotension. Although some research has found that children suffer-
A. Swaminathan et al.
ing TBI with elevated systolic blood pressures had higher survival rates, there is currently no role for inducing supranormal blood pressure (34). FURTHER MANAGEMENT IN THE EMERGENCY DEPARTMENT Before diagnostic imaging, the patient had a generalized tonic-clonic seizure. Phenobarbital was administered, with cessation of seizure activity. The patient was then transported to Radiology, where computed tomography (CT) scanning of the head, cervical spine, chest, abdomen, and pelvis were obtained. Non-contrast head CT (NCHCT) revealed multiple intracranial injuries, including left anterior and posterior subgaleal hematomas, a minimally displaced left parietal bone fracture, left epidural vs. subdural hematoma, right frontal subdural hematoma, multiple areas of subarachnoid hemorrhage, right temporal horn hemorrhagic contusion, and a left lateral ventricle interventricular hemorrhage, but no evidence of midline shift or mass effect (Figure 1). Cervical spine CT scan demonstrated no fractures, and CT scans of the chest, abdomen, and pelvis showed no injuries. On return to the ED, the patient was loaded with intravenous phenytoin for further seizure prophylaxis. OTHER ACUTE INTERVENTIONS Pediatric critical care consensus statements recommend aggressive ICP-directed therapy in all children with se-
Figure 1. Non-contrast head computed tomography scan of the patient. Thick arrow: subarachnoid hemorrhage; thin arrow: subdural hemorrhage; triangle: intraventricular blood.
Evaluation and Management of Pediatric Head Trauma
vere TBI and a GCS score ⬍ 8 (35). The literature supporting these recommendations is comprised of a number of small, single-center, observational and retrospective studies. No randomized controlled trial has been performed in any age group evaluating the effect of ICP monitoring on long-term neurologic outcomes. Intracranial hypertension is a major predictor of poor neurologic outcome and increased mortality but can be controlled with medical interventions (hyperosmolar and hyperventilation therapy) as well as surgical interventions (cerebral spinal fluid drainage and decompressive craniotomy). A discussion of these interventions is beyond the scope of this review, but it is important to appropriately identify those patients, using historical and clinical factors combined with imaging, who may require early neurosurgical intervention and aggressive ongoing management. Clinical accuracy for this, however, is limited. Open fontanels and sutures do not prevent the development of increased ICP or diminish the utility of ICP monitoring (36). Studies demonstrate that up to 86% of children with an initial GCS ⱕ 8 had ICP measurements ⬎ 20 mm Hg (37). In addition, 53– 63% of patients with severe TBI in combination with abnormal NCHCT had elevated ICP (38). A normal admission NCHCT does not rule out increased ICP (39). Non-surgical management of pediatric patients with confirmed or suspected increases in ICP can be challenging. Prophylactic use of hyperosmolar therapy (mannitol or hypertonic saline) in children with severe TBI is not advocated. Current recommendations are to use these agents only in conjunction with an ICP monitor and documented elevation in ICP (40,41). However, mannitol may be given empirically for signs and symptoms of herniation or impending herniation. This includes acute decline in mental status and unilateral dilatated and unresponsive pupil. Prophylactic anti-seizure medication is appropriate to initiate, and use of these agents should be continued for 7 days in all patients with moderate to severe head trauma defined as an initial GCS ⱕ 8 (42). No one agent has been clearly proven superior. Up to 40% of these patients will experience early posttraumatic seizures (43). The risk of seizure development increases threefold in children under the age of 2 years (vs. those older than the age of 12) (44). Seizures can cause secondary brain injury by a number of different mechanisms, including hypoxia, hypercarbia, and increased cerebral metabolic demand, and will cause further increases in ICP. Multiple studies have demonstrated reduction in the incidence of early post-traumatic seizures with the use of anti-seizure medications, but there are no well-designed studies to suggest a preferred or superior agent (42,45). It is important to remember however, that early seizure prophylaxis does not affect
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the risk of developing late post-traumatic (⬎ 7 days after event) seizures (46).
DISCUSSION The management of pediatric head trauma in the ED focuses on rapid stabilization, diagnosis, and attempts to reduce the development of secondary brain injury. Appropriate interventions can have a significant effect on neurologic outcome. Hypoxia and hypotension must be avoided or rapidly corrected due to the association of each with extremely poor outcomes. Early definitive airway control should be considered in all patients both to avoid hypoxia and facilitate further management. Hyperventilation should be avoided unless signs of herniation are present, as it has been shown to increase cerebral ischemia. Early seizure prophylaxis should be initiated in all patients with severe TBI. Finally, because many of the necessary therapeutic modalities rely on invasive monitoring, close cooperation between the emergency physician and neurosurgeon is necessary.
CONCLUSION The patient was evaluated by the neurosurgical service and it was determined that acute invasive surgical intervention was not indicated, as there was not an easily identifiable lesion causing mass effect that would be amenable to operative removal. The patient was admitted to the Pediatric Intensive Care Unit and repeat NCHCT demonstrated no change in the injury patterns previously described. On hospital day 3, the patient was successfully extubated and enteral feeds were started. Repeat NCHCT on hospital day 6 showed evidence of resolving subdural and intraventricular hemorrhage. The patient was discharged home on hospital day 7 on a phenobarbital taper. At the time, the patient showed appropriate neurological development for his age. Due to the patient’s young age, the potential for long-term neurologic sequelae remained uncertain upon discharge.
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