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Initial approach to severe traumatic brain injury in children

Official reprint from UpToDate www.uptodate.com 2013 UpToDate

Initial approach to severe traumatic brain injury in children Authors Monica S Vavilala, MD Pichaya Waitayawinyu, MD Neil M Dooney, MBBS Disclosures All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Nov 2013. | This topic last updated: jul 2, 2013. INTRODUCTION Injury is the leading cause of death for children and adolescents in the United States and most developed countries [1]. Of these deaths, about 40 percent are the result of traumatic brain injury [2]. Traumatic brain injury (TBI) is often associated with cervical spine injury [3]. The rapid identification and stabilization of children with severe traumatic brain injury is essential. Effective initial management of conditions that contribute to secondary brain injury (ie, hypoxia and hypotension) and prompt transfer to a facility that can provide pediatric trauma care are important determinants of outcome. This topic will review the initial evaluation and management of children with severe traumatic brain injury (TBI). The evaluation and management of minor head injury, inflicted head injury, and elevated intracranial pressure are discussed separately. (See "Minor head trauma in infants and children" and "Child abuse: Evaluation and diagnosis of abusive head trauma in infants and children" and "Elevated intracranial pressure (ICP) in children".) DEFINITIONS Severity of traumatic brain injury (TBI) is typically defined by the initial Glasgow Coma Scale (GCS) score. The GCS score is a widely used assessment of neurological function that has been validated in many studies since it was first introduced in 1976 [4]. It has been modified for use in children (table 1). Severity of TBI as determined by initial GCS score is as follows: Mild (GCS score 13 to 15) Moderate (GCS score 9 to 12) Severe (GCS score <9) Other factors at the initial assessment that have been used to identify patients with severe injury include the Pediatric Trauma Score (as a proxy for other major injuries) and the presence of hypotension and/or hypoxemia (table 2). (See "Classification of trauma in children".) EPIDEMIOLOGY Head injury occurs commonly in children. Among children 0 to 14 years of age in the United States, traumatic brain injury (TBI) accounted for approximately 475,000 emergency department visits per year between 1995 and 2001 [2]. In 2000, about 50,000 children 17 years of age were hospitalized for TBI [5]. Of these, 29 percent were 4 years of age, and 52 percent were between 10 and 17 years of age. Various mechanisms result in TBI severe enough to require hospitalization. Among children less than four years of age, falls accounted for 41 percent of injuries in one series [2]. In comparison, motor vehicle-traffic incidents caused 43 percent of injuries among adolescents. Inflicted head injury is a significant mechanism, particularly for infants less than one year of age. Of children less than one year of age in the United Kingdom who were admitted to intensive care units with head injuries, 52 percent had been assaulted [6]. (See "Child abuse: Epidemiology, mechanisms, and types of abusive head trauma in infants and children".)
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Section Editor Richard G Bachur, MD

Deputy Editor James F Wiley, II, MD, MPH

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Initial approach to severe traumatic brain injury in children

Among all children presenting to the emergency department in one prospective series, 98 percent had a Glasgow Coma Scale (GCS) score of 15, suggesting that most head injuries are minor [7]. However, approximately 75 percent of children with multiple trauma have TBI and almost 80 percent of all trauma deaths are associated with TBI [8,9]. Mortality rates between 17 and 33 percent have been reported in retrospective series describing children with severe brain injury [10-13]. In developed countries, TBI is the most common cause of death and disability in childhood [1,14]. Approximately 3000 children die each year of head injuries in the United States [2]. The highest pediatric morbidity and mortality is reported in children younger than four years of age, and in those with low Glasgow Coma Scale (GCS) scores at initial presentation, coagulopathy, hyperglycemia, and hypotension [10,14-21]. Overall mortality among children with TBI who are treated in emergency departments or require hospital admission is 4.5 percent (compared with 10.4 percent among adults) [22]. Despite the higher survival in children with TBI, disability is significant, and the functional long-term outcome appears to be related to severity of initial injury [23]. TYPES OF BRAIN INJURY Diffuse brain injury (DBI) is the most common type of severe traumatic brain injury in children and is usually produced by acceleration or deceleration forces [24]. The mildest form of DBI is a concussion. (See "Minor head trauma in infants and children", section on 'Concussion' and "Concussion and mild traumatic brain injury", section on 'Clinical features' and "Concussion and mild traumatic brain injury", section on 'Sequelae'.) Diffuse axonal injury (DAI) is a more severe form of diffuse brain injury. DAI develops as the result of tissue shearing at the interface of grey and white matter. It can occur in association with focal injuries. Focal injuries include brain contusions and intracranial hemorrhage. An acceleration or deceleration injury can result in a cerebral contusion. Contusions may be in the location of impact (coup), or on the opposite side of the brain (contrecoup), or both. Intracranial hemorrhage may occur from either blunt or penetrating trauma. Epidural hematoma, subdural hematoma, or subarachnoid hemorrhage usually occurs as the result of blunt trauma. In children, an epidural hematoma may arise from the middle meningeal artery, the middle meningeal vein, diploic veins, or venous sinuses [25]. A subdural hematoma results from rupture of bridging veins. Subarachnoid hemorrhage develops from tearing of small vessels in the pia mater. Subdural hematoma and subarachnoid hemorrhage usually occur as the result of severe trauma and are frequently associated with other intracranial injuries. ASSOCIATED INJURIES Multiple trauma is common among children with severe traumatic brain injury [11,26]. In one retrospective series describing severely head injured children, 39 percent had sustained multiple trauma [11]. In these cases, death is typically a result of the head injury [13,27]. Cervical spine injury (CSI) must always be suspected for children with traumatic brain injury or injury above the clavicle. Although CSI in children is uncommon, approximately one-half of patients with CSI have concomitant TBI [3]. Cervical spine injury in children is reviewed elsewhere. (See "Evaluation of cervical spine injuries in children and adolescents".) PATHOPHYSIOLOGY The pathophysiology of severe TBI involves two insults. The primary event is the direct injury to brain parenchyma. A cascade of biochemical, cellular, and metabolic responses causes secondary damage. Secondary injury also occurs as the result of exogenous insults, such as hypoxia and hypotension. Initially following brain injury, cerebral blood flow appears to be decreased in children (rather than increased, as previously thought) [28-30]. Hypoperfusion in conjunction with increased metabolic demand makes the brain more susceptible to secondary insults, such as hypoxemia and hypotension. Cerebral perfusion may be particularly dependent on maintaining adequate blood pressure because cerebral autoregulation is often impaired following severe pediatric TBI [12,31]. In addition, release of excitatory neurotransmitters, such as acetylcholine, glutamate, and aspartate causes neuronal damage [32]. Following this initial phase, cerebral swelling develops that generally peaks 24 to 72 hours after the injury. The resulting intracranial hypertension can further compromise cerebral perfusion leading to more ischemia, swelling,
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Initial approach to severe traumatic brain injury in children

herniation, and death. Diffuse cerebral swelling following severe traumatic brain injury is more common among infants and children as compared with adults [33]. Mechanisms that account for this age-related difference are not known. Anatomical and pathophysiological factors likely play a role. As an example, a diffuse pattern of brain injury may develop because the infant skull is more compliant and can tolerate considerable deformation before fracture occurs [34,35]. In addition, brain atrophy that probably begins in young adulthood, allows for more room in the adult skull for the brain to expand. Finally, experimental data from animals suggest that pathophysiological features, such as enhanced diffusion of excitotoxic neurotransmitters, the inflammatory response of the developing brain, and changes in bloodbrain-barrier permeability may also be involved [36]. The volume relationships between brain parenchyma, cerebrospinal fluid, and blood, as well as physiologic mechanisms that maintain pressure homeostasis (including the autoregulation of cerebral blood flow to maintain cerebral perfusion pressure) within the intracranial compartment are discussed separately. (See "Elevated intracranial pressure (ICP) in children", section on 'Physiology'.) EVALUATION Children with severe traumatic brain injury must be promptly recognized and their conditions emergently stabilized in order to limit secondary brain injury and improve outcomes. Injuries that require immediate neurosurgical intervention and associated injuries that may impact management must also be identified. A systematic primary survey to rapidly identify and treat potentially fatal conditions, such as airway compromise, impaired respiratory mechanics, and hemorrhagic shock should be initially performed. This should be followed by a secondary survey that includes a fully exposed head-to-toe examination of the child, with a neurological assessment. An initial approach to the injured child that includes a detailed description of the primary and secondary surveys, as well as prehospital preparation, is presented elsewhere. (See "Classification of trauma in children".) The assessment of airway, ventilatory, and circulatory function in children is reviewed separately. (See "Initial assessment and stabilization of children with respiratory or circulatory compromise", section on 'Evaluation' and "Emergent endotracheal intubation in children" and "Assessment of perfusion in pediatric resuscitation".) The remainder of this discussion will focus on the evaluation specific to head injured patients, including the recognition of signs and symptoms that may adversely affect outcome. History For most children with severe traumatic brain injury (TBI), the history of the injury will be straightforward. A notable exception is for the child who has sustained an inflicted head injury. In this situation, there is often no history of a traumatic event, despite evidence of significant brain injury. The evaluation and diagnosis of inflicted head injury is discussed separately. (See "Child abuse: Evaluation and diagnosis of abusive head trauma in infants and children".) Historical features may also identify children who do not appear to have had a significant head injury, but have in fact, sustained a severe TBI and whose condition may deteriorate. In addition to mechanism of injury, other features to consider include the following [37]: Prolonged loss of consciousness and/or abnormal mental status Persistent vomiting Severe headache Progression of symptoms Physical examination General assessment Vital signs must include pulse oximetry and an assessment of ventilation (chest wall movement, breath sounds, or end tidal CO2 measurement). Hypoxia and hypotension should be immediately identified and treated. Respiratory depression, bradycardia, and/or hypertension may indicate impending herniation, which must also be promptly treated. (See "Elevated intracranial pressure (ICP) in children", section on
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Initial approach to severe traumatic brain injury in children

'Herniation'.) Under most circumstances, cervical spine immobilization should be maintained throughout the evaluation, since an adequate examination to exclude cervical spine injury can rarely be performed in children with severe TBI. (See "Pediatric cervical spine immobilization" and "Evaluation of cervical spine injuries in children and adolescents".) Open wounds to the head and neck, including penetrating wounds, should be identified during the secondary survey. Management of these injuries may require surgery. In addition, children may lose significant amounts of blood from scalp lacerations. Neurological assessment The initial assessment of the child with severe TBI should include a focused neurological examination and assignment of a Glasgow Coma Scale (GCS) score (table 1). A focused neurologic examination should include the following: Level of consciousness Pupillary examination for size, reactivity, and symmetry Extraocular movements Funduscopic examination Brainstem reflexes (corneal and gag reflexes) Deep tendon reflexes Response to pain Any abnormalities in this examination may suggest increased intracranial pressure (ICP) with impending transtentorial herniation that may require immediate intervention. (See 'Management' below and "Evaluation of stupor and coma in children", section on 'Transtentorial herniation'.) Signs of herniation that must be recognized include the following: Signs of uncal herniation including a third cranial nerve palsy, followed immediately by hemiplegia. Progressive changes in respiratory pattern, pupil size, vestibuloocular reflexes, and posture that correlate with the anatomic level of brain involvement (figure 1). Cushing's triad, which includes hypertension, bradycardia, and slow irregular respirations. Laboratory studies Laboratory evaluation depends upon the type and extent of injuries identified during the primary and secondary surveys. At minimum, most children with multiple injuries require a hematocrit, type and screen, and urinalysis. (See "Trauma management: Approach to the unstable child", section on 'Laboratory studies' and "Approach to the initially stable child with blunt or penetrating injury".) Laboratory tests that may be useful for the management of children with severe TBI include blood glucose (hyperglycemia is a poor prognostic indicator for children with severe TBI) and serum electrolytes with osmolarity. A panel of coagulation studies may be useful in some patients as an indicator of severity of injury. DIC has been associated with poor outcomes in children with severe TBI [11]. (See "Disseminated intravascular coagulation in infants and children", section on 'Diagnosis'.) Imaging Computed tomography (CT) of the head is the preferred initial imaging modality for children with severe traumatic brain injury. Any lesion that requires emergent surgery is reliably identified by CT. There may also be a role for early MRI in the diagnosis and treatment of TBI but this practice is not standard. (See "Approach to neuroimaging in children", section on 'MRI applications'.) By definition, all children with moderate to severe TBI have an abnormal neurologic evaluation and should receive CT following initial evaluation and stabilization. (See 'Definitions' above.) The indications for obtaining imaging studies for children with apparent mild head injury are reviewed elsewhere.
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Initial approach to severe traumatic brain injury in children

(See "Minor head trauma in infants and children", section on 'Indications for neuroimaging'.) Focal injuries, such as contusions and hemorrhage, are readily diagnosed by CT. Patients with diffuse axonal injury (DAI) may initially have a normal CT scan but generally have significant neurologic findings on physical examination. Magnetic resonance imaging is more sensitive for DAI but is usually not necessary for initial stabilization and treatment. A repeat CT scan often shows secondary injury due to cerebral edema. The most common finding on CT scan in children with TBI is diffuse cerebral swelling [24]. MANAGEMENT The initial management of children with severe traumatic brain injury (TBI) includes meticulous attention to support of airway, breathing, and circulation in order to prevent secondary injury. Specific therapies may be initiated as indicated to minimize and/or treat increased intracranial pressure (ICP). (See 'Pathophysiology' above.) In many children with severe traumatic brain injury, life-saving supportive therapies are initiated by emergency clinicians. Whenever possible, these patients should then be managed by specialists with pediatric expertise, including neurosurgeons and intensivists. Airway and breathing General principles of airway management for children (including techniques for opening and maintaining an airway, bag-mask ventilation, and tracheal intubation) are reviewed elsewhere. (See "Basic airway management in children" and "Emergent endotracheal intubation in children".) Specific considerations for the management of airway and breathing for children with severe TBI are discussed here. The child who is lucid and has a normal blood pressure can be managed with supplemental oxygen alone. Advanced airway management, including tracheal intubation, may be required to maximize oxygenation and ventilation and protect against aspiration of gastric contents in the following situations: Decreasing level of consciousness (GCS <9) Marked respiratory distress Hemodynamic instability Cervical spine immobilization must be maintained while airway procedures are being performed. (See "Pediatric cervical spine immobilization", section on 'Airway management'.) Considerations for tracheal intubation for children with traumatic brain injury include the following: Nasotracheal intubation should not be performed in patients with midface trauma or signs of a basilar skull fracture (raccoon's eyes, mastoid hematoma, or CSF drainage from the nose or ear canals). Children with these injuries may have fractures of the cribriform plate. We generally use cuffed tracheal tubes for all major pediatric trauma to protect the airway from aspiration. (See "Emergent endotracheal intubation in children", section on 'Cuffed versus uncuffed'.) Rapid sequence intubation Unless consciousness is severely depressed, endotracheal intubation is accomplished by using a rapid-sequence technique with application of cricoid pressure and preoxygenation (table 3) (see "Rapid sequence intubation (RSI) in children") as follows: Pretreatment Lidocaine may minimize any increase in intracranial pressure that can be associated with airway manipulation. (See "Rapid sequence intubation (RSI) in children", section on 'Lidocaine'.) Sedative agents Etomidate and thiopental have neuroprotective properties. Thiopental causes vasodilatation and myocardial depression, resulting in a decrease in systolic blood pressure and should not be used in patients who are hemodynamically unstable. Etomidate is frequently used during RSI in children with severe traumatic brain injury; although etomidate can cause transient adrenal suppression, the benefits appear to outweigh the risks in most patients. (See "Rapid sequence intubation (RSI) in children", section on 'Sedative and induction agents'.)
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Initial approach to severe traumatic brain injury in children

Paralytic agents Although increased ICP with the use of succinylcholine has been reported in patients with brain tumors, there is no definitive evidence that succinylcholine causes a rise in ICP in humans with brain injury [38,39]. Factors that must be considered in choosing between succinylcholine and rocuronium include the risk of succinylcholine for children with undiagnosed neuromuscular conditions and the longer duration of paralysis with rocuronium for those who may have a difficult airway. (See "Rapid sequence intubation (RSI) in children", section on 'Paralysis'.) Ventilation Hyperventilation (PaCO2 <35 mmHg) may cause cerebral ischemia as the result of decreased cerebral blood flow [30,40]. Consequently, PaCO2 should be maintained between 35 and 38 mmHg unless there are signs of pending herniation [41]. (See 'Neurological assessment' above and 'Management' above.) Fluid management General principles of the management of hypovolemic and hemorrhagic shock in children, as well as techniques for vascular access, are discussed separately. (See "Vascular (venous) access for pediatric resuscitation and other pediatric emergencies" and "Hypovolemic shock in children: Initial evaluation and management", section on 'Fluid resuscitation'.) In general, isotonic fluids are preferred to hypotonic fluids. Adult data suggest that albumin may be harmful after TBI [42]. Specific considerations for fluid management for children with severe TBI are discussed here. Outcomes for children with severe TBI who are hypotensive at the initial evaluation are typically poor [10,12,14,20,43-45]. Volume should be restored. Isotonic solutions should be used for fluid resuscitation. Blood products should be administered as indicated. For example, in one observational study of 118 children with moderate to severe traumatic brain injury and documented hypotension, fluid therapy during early resuscitation was associated with significantly lower mortality (30 percent [17 of 57 patients] versus 56 percent [34 of 61 patients]) and significantly better functional neurologic outcome [43]. The target blood pressure required to maintain the minimum cerebral perfusion pressure necessary to meet cerebral metabolic demands in infants and children has not been established and may be an age dependent continuum. Systolic blood pressures should be maintained above the fifth percentile for age and gender at the very least [46]. However, improved outcomes have been reported for patients with substantially higher initial blood pressures [10,12]. Other initial management considerations Interventions that are typically used to treat children with severe traumatic brain injury improve intermediate outcomes, such as intracranial pressure, cerebral oxygen consumption, and cerebral blood flow. Evidence that these treatments improve long-term clinical outcomes is therefore largely indirect. Head positioning The head should be maintained in a neutral position to avoid jugular venous obstruction. In prospective observational studies, elevating the head to 30 degrees appears to optimize cerebral perfusion pressure and decrease ICP for adult patients, provided that mean arterial pressure is maintained [47,48]. There are no data regarding the efficacy of this intervention for children. Sedation and neuromuscular blockade Adequate sedation and pharmacologic paralysis facilitate the safe transportation of intubated children with severe TBI. Oxygenation, ventilation, and blood pressure must be vigilantly monitored for patients who are sedated, with or without paralysis. Limited evidence suggests that cerebral oxygen consumption may be decreased in patients receiving neuromuscular blockade [49]. Antiseizure prophylaxis Prophylactic treatment with anticonvulsants reduces the incidence of early posttraumatic seizures among children with severe TBI [50,51]. Seizures immediately following severe traumatic brain injury may increase brain metabolic demands and increase ICP, leading to secondary brain injury [41]. In addition, retrospective studies have demonstrated improved outcomes among children with TBI who were treated with anticonvulsants [52,53]. Experts suggest that children receive anticonvulsant therapy during the first week following severe TBI [54].
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Initial approach to severe traumatic brain injury in children

Hyperthermia Hyperthermia should be aggressively prevented and treated [55]. Hyperosmolar therapy Randomized trials, observational reports, and extensive clinical experience have demonstrated that hyperosmolar therapy effectively decreases increased intracranial pressure in children with TBI [56-62]. Options include hypertonic saline and mannitol: Hypertonic saline Evidence from small randomized trials and observational reports suggests that hypertonic saline, administered either as a bolus or a constant infusion, is effective for reducing intracranial pressure [58-62]. Adverse effects related to therapy with hypertonic saline include rebound intracranial hypertension, central pontine myelinolysis, and subarachnoid hemorrhage [63]. (See "Elevated intracranial pressure (ICP) in children", section on 'Mannitol'.) Mannitol The effectiveness of mannitol for decreasing intracranial pressure among patients with traumatic brain injury has been demonstrated by extensive clinical experience and in several small series describing adult and pediatric patients [56,57]. Nephrotoxicity can occur with mannitol therapy, particularly if patients become hypovolemic [64]. Hyperventilation Although hyperventilation reduces intracranial pressure, indirect evidence suggests that routine hyperventilation may be harmful for patients with TBI. Hyperventilation produces hypocapnia which causes vasoconstriction and decreased cerebral blood flow (CBF) [65,66]. Decreased CBF has been associated with poor outcomes among children with TBI [30], and severe hypocapnia (PaCO2 <30 mmHg) has been associated with increased mortality [67]. Patients should only receive temporary hyperventilation (to reduce PaCO2 to less than 35 mmHg) with signs and symptoms of impending herniation [41]. (See "Elevated intracranial pressure (ICP) in children", section on 'Hyperventilation'.) Glucose Hyperglycemia has been associated with poor outcomes for children and adults with TBI [11,15,68,69]. This may be because hyperglycemia (as the result of a stress response) is a marker for severity of injury and/or elevated blood sugar contributes to poor outcome by worsening brain tissue lactic acidosis [70-73]. In an observational study of 101 children under 14 years of age who underwent emergent craniotomy for TBI, perioperative hyperglycemia (serum glucose 200 mg/dL [11.1 mmol/L]) was found in 45 percent of children and was significantly associated with age <4 years, GCS 8, and the presence of multiple traumatic lesions, including subdural hematoma [74]. We typically maintain glucose levels 200 mg/dL for head injured children. Corticosteroids Limited evidence does not support a benefit for treatment with corticosteroids for head injured patients. In addition, a large, prospective, multicenter trial described increased mortality among patients with acute traumatic brain injury who received corticosteroids [75]. (See "Elevated intracranial pressure (ICP) in children", section on 'Corticosteroids'.) Hypothermia Hypothermia for children with severe traumatic brain injury is not beneficial and may be harmful and should not be performed. (See "Elevated intracranial pressure (ICP) in children", section on 'Contraindicated therapies'.) Burr hole Rarely, a patient with an epidural hematoma may require emergent drainage through a burr hole. This procedure should be done by a neurosurgeon whenever possible. Monitoring Initial monitoring of the child with severe TBI includes measurement of heart rate, blood pressure, and pulse oximetry. Capnography should be used (when available) to monitor end-tidal CO2 to avoid excessive hyperventilation for patients who require controlled ventilation. If end-tidal CO2 is to be used as the primary monitor for ventilation, an initial determination of arterial pCO2 should also be performed to ensure that end tidal and arterial CO2 are correlating well [76]. Intracranial pressure monitoring is generally recommended for children who have an abnormal initial head CT and an initial GCS score between 3 and 8 [77]. Interventions that have been effective for decreasing ICP (ie, hyperosmolar therapy, decompressive craniotomy, and hyperventilation) require accurate and continuous monitoring of intracranial
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Initial approach to severe traumatic brain injury in children

pressure [61,78,79]. ICP monitoring is usually not initiated in the emergency department. However, children who may need ICP monitoring should be admitted to a pediatric intensive care unit at a trauma center. Initial management decisions The immediate management of a child with severe traumatic brain injury (GCS score 8) (table 1), or with moderate injury (GCS score between 9 and 12) (table 1) whose condition is deteriorating or has associated injuries should include the following : Focal injuries that may require neurosurgical intervention (ie, penetrating injuries, epidural hematomas, or subdural hematoma) must be quickly identified. (See 'Evaluation' above.) Immediate neurosurgical consultation should be requested for children with focal injuries who have signs of increased intracranial pressure on physical examination or imaging studies. (See 'Neurological assessment' above.) Children with GCS scores 8 or with GCS scores between 9 and 12 whose conditions are deteriorating should undergo endotracheal intubation. Intubation should also be considered for those with GCS scores between 9 and 12 who cannot protect their airways or are being transported out of the emergency department. (See 'Rapid sequence intubation' above.) Children with signs of herniation should be treated as follows (figure 1) (see 'Other initial management considerations' above): Assure adequate oxygenation, breathing, and blood pressure. Give hyperosmolar therapy. Provide mild hyperventilation (PaCO2 30 to 35 mmHg) for children who do not respond to hyperosmolar therapy. Request immediate neurosurgical evaluation. DISPOSITION Outcomes appear to be improved for children with severe pediatric traumatic brain injury (TBI) who are treated at trauma centers with expertise in caring for children [80,81]. Experts recommend that patients in the field with a GCS 12 or Pediatric Trauma Score 8 be transported directly to a pediatric trauma center whenever possible (table 2) [82-85]. Children who are initially treated at a community hospital who should be transferred to a pediatric trauma center once their conditions are stabilized include the following: GCS 8 GCS 12 with associated major injuries Deterioration in clinical condition, including decrease in GCS INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, The Basics and Beyond the Basics. The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon. Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on patient info and the keyword(s) of interest.) Basics topic (see "Patient information: Closed head injury (The Basics)")
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Initial approach to severe traumatic brain injury in children

SUMMARY AND RECOMMENDATIONS The rapid identification and stabilization of children with severe traumatic brain injury is essential for the effective initial management of focal injuries and conditions that contribute to secondary brain injury (ie, hypoxia and hypotension). Prompt transfer to a facility that can provide pediatric trauma care is an important determinant of outcome. Severe traumatic brain injury (TBI) is defined by an initial Glasgow coma scale (GCS) score <9. Patients with moderate TBI have GCS scores between 9 and 12. Associated injuries also contribute to poor outcomes. (See 'Definitions' above.) Causes of severe TBI in children include falls, motor vehicle-traffic incidents, and inflicted head injury. (See 'Epidemiology' above.) Types of brain injury include diffuse brain injury (including diffuse axonal injury) and focal injuries, such as contusions or hemorrhage. Children with severe TBIs often have associated injuries. (See 'Types of brain injury' above and 'Associated injuries' above.) Brain injury occurs as a result of the primary injury and secondary events including the brain's response to the injury and exogenous insults, such as hypoxia and hypotension. (See 'Pathophysiology' above.) Evaluation includes a primary assessment to identify life-threatening injuries, followed by a thorough physical examination. A GCS score and focused neurological examination should be performed. Initial imaging for head injury should be with computed tomography. (See 'Evaluation' above.). Management of severe TBI includes aggressively maintaining oxygenation, ventilation, and blood pressure. Other management considerations include the following (see 'Management' above): The head should be elevated to 30 degrees, provided that means arterial pressure can be maintained. We suggest that children with severe TBI receive anticonvulsants to prevent early posttraumatic seizures (Grade 2C). Immediate management decisions include indications for intubation and emergent neurosurgical consultation. (See 'Initial management decisions' above.) Impending herniation is an emergency. We suggest that patients with signs of impending herniation be treated initially with hyperosmolar therapy rather than hyperventilation (Grade 2C). We prefer mannitol to hypertonic saline for initial management. We suggest that patients who do not respond to hyperosmolar therapy be treated with hyperventilation (PaCO2 30 to 35) (Grade 2C). (See 'Initial management decisions' above.) Children with severe TBI or those with moderate TBI who have associated injuries or whose clinical condition is deteriorating should be treated at a trauma center with pediatric capability whenever possible. Use of UpToDate is subject to the Subscription and License Agreement. REFERENCES 1. Krug EG, Sharma GK, Lozano R. The global burden of injuries. Am J Public Health 2000; 90:523. 2. Langlois, JA, Rutland-Brown, W, Thomas, KE. Traumatic brain injury in the United States: emergency department visits, hospitalizations, and deaths. Centers for Disease Control and Prevention, National Center for Injury Prevention and Control, Atlanta 2006. 3. Brown RL, Brunn MA, Garcia VF. Cervical spine injuries in children: a review of 103 patients treated consecutively at a level 1 pediatric trauma center. J Pediatr Surg 2001; 36:1107.
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28. Zwienenberg M, Muizelaar JP. Severe pediatric head injury: the role of hyperemia revisited. J Neurotrauma 1999; 16:937. 29. Sharples PM, Stuart AG, Matthews DS, et al. Cerebral blood flow and metabolism in children with severe head injury. Part 1: Relation to age, Glasgow coma score, outcome, intracranial pressure, and time after injury. J Neurol Neurosurg Psychiatry 1995; 58:145. 30. Adelson PD, Clyde B, Kochanek PM, et al. Cerebrovascular response in infants and young children following severe traumatic brain injury: a preliminary report. Pediatr Neurosurg 1997; 26:200. 31. Vavilala MS, Muangman S, Tontisirin N, et al. Impaired cerebral autoregulation and 6-month outcome in children with severe traumatic brain injury: preliminary findings. Dev Neurosci 2006; 28:348. 32. Ruppel RA, Kochanek PM, Adelson PD, et al. Excitatory amino acid concentrations in ventricular cerebrospinal fluid after severe traumatic brain injury in infants and children: the role of child abuse. J Pediatr 2001; 138:18. 33. Lang DA, Teasdale GM, Macpherson P, Lawrence A. Diffuse brain swelling after head injury: more often malignant in adults than children? J Neurosurg 1994; 80:675. 34. Margulies SS, Thibault KL. Infant skull and suture properties: measurements and implications for mechanisms of pediatric brain injury. J Biomech Eng 2000; 122:364. 35. Coats B, Margulies SS. Material properties of human infant skull and suture at high rates. J Neurotrauma 2006; 23:1222. 36. Kochanek PM. Pediatric traumatic brain injury: quo vadis? Dev Neurosci 2006; 28:244. 37. Palchak MJ, Holmes JF, Vance CW, et al. A decision rule for identifying children at low risk for brain injuries after blunt head trauma. Ann Emerg Med 2003; 42:492. 38. 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. 39. 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. 40. Stocchetti N, Maas AI, Chieregato A, van der Plas AA. Hyperventilation in head injury: a review. Chest 2005; 127:1812. 41. Mazzola CA, Adelson PD. Critical care management of head trauma in children. Crit Care Med 2002; 30:S393. 42. Finfer S, Bellomo R, Boyce N, et al. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med 2004; 350:2247. 43. Zebrack M, Dandoy C, Hansen K, et al. Early resuscitation of children with moderate-to-severe traumatic brain injury. Pediatrics 2009; 124:56. 44. Samant UB 4th, Mack CD, Koepsell T, et al. Time of hypotension and discharge outcome in children with severe traumatic brain injury. J Neurotrauma 2008; 25:495. 45. Chaiwat O, Sharma D, Udomphorn Y, et al. Cerebral hemodynamic predictors of poor 6-month Glasgow Outcome Score in severe pediatric traumatic brain injury. J Neurotrauma 2009; 26:657. 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 4. Resuscitation of blood pressure and oxygenation and prehospital brain-specific therapies for the severe pediatric traumatic brain injury patient. Pediatr Crit Care Med 2003; 4:S428. 47. Feldman Z, Kanter MJ, Robertson CS, et al. Effect of head elevation on intracranial pressure, cerebral perfusion pressure, and cerebral blood flow in head-injured patients. J Neurosurg 1992; 76:207. 48. Ng I, Lim J, Wong HB. Effects of head posture on cerebral hemodynamics: its influences on intracranial pressure, cerebral perfusion pressure, and cerebral oxygenation. Neurosurgery 2004; 54:593. 49. Vernon DD, Witte MK. Effect of neuromuscular blockade on oxygen consumption and energy expenditure in sedated, mechanically ventilated children. Crit Care Med 2000; 28:1569.
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