Severe Pediatric Traumatic Brain Injury

      Traumatic brain injuries (TBI) affect 475,000 children under age 14 each year in the United States alone. Ninety percent of patients are treated in emergency departments and released; however, more than 47,000 hospitalizations per year are a direct result of these injuries. On average, 2,685 children die annually from traumatic brain injuries, and more than 30,000 children per year acquire lifelong disabilities. With proper prehospital care of these severely injured children, we can reduce secondary injury and maximize survival and good neurological outcomes.

EPIDEMIOLOGY

   Children comprise two of three age groups most prone to traumatic brain injuries. In particular, children younger than five years and adolescents to young adults 15 to 24 years are most vulnerable, due to exploration and lack of coordination in young children and risk-taking behaviors in adolescents.

   The most common causes of traumatic brain injuries in the United States, in order of prevalence, include falls, motor vehicle collisions and struck by/against events. TBIs occur in toddlers falling down stairs, as well as from non-accidental trauma such as shaken-baby syndrome. Adolescents and young adults sustain traumatic brain injuries from motor vehicle collisions; sports injuries like skiing/snowboarding, football, ATV/snowmobile riding and trampoline use; and other causes. Alcohol experimentation is involved in a number of incidents. This paper specifically addresses current recommendations for prehospital management of pediatric severe traumatic brain injury (GCS less than 9) in order to maximize outcomes.

BRAIN INJURIES

   Traumatic brain injury is a spectrum of insults to the brain. Epidural hematoma occurs when damage to a meningeal or other artery causes bleeding between the skull and dura. These patients classically present with a lucid interval prior to becoming rapidly unresponsive. Subdural hematoma results from injury to the bridging vessels between the dura and brain. These bleeds may be self-limited or extensive, causing massive cerebral shifting. Intraparenchymal hemorrhage results from injury to the vessels within the brain itself, causing bleeding within one or multiple spots within the brain matter. Lastly, diffuse axonal injury (DAI) is microscopic damage to the axons of the brain nerves. This type of injury is most common in traumatic brain injuries, is not seen on CT-scanning and can result in devastating outcomes. All of these injuries can cause cerebral edema, further worsening patient outcome.

   Numerous multidisciplinary teams have been formed to provide guidelines for management of both adult and pediatric severe TBI. Specific guidelines for management of pediatric TBI include Guidelines for the Acute Medical Management of Severe Traumatic Brain Injuries in Infants, Children, and Adolescents.¹ More recent recommendations published in December 2007 include An Evidence-based Approach to Severe Traumatic Brain Injury in Children.² Several other groups have also published guidelines that encompass pediatric care.^3,4

AIRWAY MANAGEMENT

   As with all trauma patients, cervical spine immobilization should be established immediately. This is especially true in pediatric trauma care, as the majority of spinal cord injuries in children are to the cervical spine. This is due to a relatively large head, weak neck musculature and ligaments, and incomplete ossification of the vertebrae.

   Endotracheal intubation was once thought to be the mainstay of airway management for traumatic brain injuries. Several studies have brought this mind-set into question. One retrospective study of rural EMS endotracheal intubation attempts in 105 pediatric trauma patients found that only 9.3% of patients could not be ventilated or oxygenated by bag-valve mask (BVM) alone.⁵ Furthermore, multiple intubation attempts were associated with transport delays and lower discharge Glasgow Coma Scale (GCS) scores. Gausche, et al., in a prospective, randomized trial demonstrated no difference in outcomes in TBI patients, but fewer complications with BVM in general trauma. Current guidelines do not recommend endotracheal intubation over bag-valve mask ventilation in prehospital care. Some indicators suggesting a potential need for intubation include a GCS under 9 (severe TBI), hypoxemia, hypercarbia, aspiration or signs of elevated intracranial pressure.

   If intubation is indicated, proper endotracheal tube sizing is key in pediatric airway management (see Figure 1). The depth of the endotracheal tube should be three times the size of the tube (i.e., a 4mm ETT should be placed at 12cm depth). The tube should not be secured around the neck, as this can reduce venous outflow and cause increased intracranial vascular congestion. Confirm endotracheal tube placement by both auscultation and end-tidal carbon dioxide capnography (EtCO₂).

   Rapid sequence intubation (RSI) is practiced as an adjunct for safer and more effective endotracheal intubation. If pediatric intubation is required for TBI care, there are no set guidelines for selecting sedatives and paralytics. In general, it is thought that medications like ketamine that cause increased intracranial pressure should be avoided. Figure 2 lists appropriate weight-based dosing of sedatives and paralytics. Care should be taken to use midazolam only in hemodynamically normal patients, as it may lower blood pressure. Etomidate and thiopental are ultrafast-acting and are thought to quickly reduce cerebral metabolism and blunt increased intracranial pressure associated with direct laryngoscopy. This transient increase in intracranial pressure, however, has not been shown to be detrimental in TBI patients. Premedication with lidocaine or fentanyl has not demonstrated a reduction in morbidity or mortality, so there is insufficient evidence to recommend for or against prehospital use.

BREATHING

   The essence of pediatric TBI respiratory care involves maintaining proper oxygenation and ventilation. In general, an adult or pediatric bag-valve mask should be used to assure adequate chest rise. Neonatal bag-valve masks are no longer recommended in any prehospital pediatric care according to the American Heart Association's 2005 Pediatric Advanced Life Support Guidelines. Proper BVM skills are necessary to avoid prehospital hypoxia.

   Hypoxia, defined as a SpO₂ (pulse oximetry) of less than 90%, increases the probability of a poor outcome by two to four times. Cerebral hypoxia is more strongly associated with poor outcome than mechanism of injury. Hypoxia occurs more rapidly in the pediatric population due to lower functional residual capacity (FRC) in the lungs and requires close monitoring to avoid such episodes. The hypoxic episode does not have to be of set duration to cause secondary injury to the brain, but rather a single documented episode of SpO₂ &llt;90% is sufficient to increase morbidity and mortality. When evaluating for hypoxemia, remember that central cyanosis is not an early or reliable indicator in children!

   Guidelines recommend 100% supplemental oxygen via non-rebreather mask, BVM or advanced airway for all TBI patients. Continuous pulse oximetry should be used at all times with a goal SpO₂ of greater than 95%. This allows a cushion for intervention prior to true hypoxia occurring. Remember that pulse oximetry lags true blood oxygen saturation by up to one minute. Hypoxia should be avoided and promptly corrected if present.

   Hypoventilation, defined as an ineffective respiratory rate, shallow breathing, irregular breathing, apneic periods or measured hypercarbia, should also be avoided or corrected promptly if present in pediatric TBI resuscitation. Continuous EtCO₂ capnography should be obtained on all severe TBI patients with the goal of keeping the patient eucapneic (EtCO₂ 35-40 mmHg) with ventilation.

   Hyperventilation, defined as an EtCO₂ of less than 35 mmHg, should also be avoided in prehospital TBI care. Inadvertent overventilation of pediatric severe TBI patients occurs frequently in both the prehospital and hospital settings. Transient hyperventilation, or bridging hyperventilation, is only indicated in the setting of clinical signs of cerebral herniation, which include extensor (decerebrate) posturing, flaccid response (1 on GCS motor score), asymmetric pupils, dilated and non-reactive pupils, or a decrease in GCS of more than two from prior best score (in patients with an initial GCS less than 9). After normo-ventilation, normotension and adequate oxygenation are assured, transient hyperventilation with a goal EtCO₂ of 30-35 mmHg should occur. This bridging should continue until clinical signs of cerebral herniation resolve or definitive treatment for increased intracranial pressure occurs. Care should be taken when ventilating the pediatric TBI patient, as the difference between ventilation rates for eucapnea and hyperventilation are subtle (see Figure 3). This further stresses the importance of accurate, constant EtCO₂ capnography to tailor care. Initial ventilation should deliver, in general, a tidal volume of 6-7 cc/kg over one second for each ventilation.

CIRCULATION

   Much like hypoxia, the detrimental effects of hypotension in the pediatric severe TBI patient can be avoided or promptly corrected. Hypotension occurs in both the prehospital and hospital arenas. One episode of hypotension not related to duration of the episode has a greater deleterious effect on pediatric patients than on adults. The goals of fluid resuscitation include maintaining a systolic blood pressure above the fifth percentile for that patient's age. Simple calculations can be used to remember the age-related cut-offs for both normal SBP and the clinical definition of pediatric hypotension (less than fifth percentile) (Figure 4).

   The role of mean arterial pressure (MAP) has not been defined in pediatric traumatic brain injury resuscitation. Cerebral perfusion pressure (CPP) is dependent on MAP minus intracranial pressure (ICP): CPP=MAP-ICP. As ICP increases in traumatic brain injury, so too must MAP be managed in order to keep the cerebral perfusion pressure greater than 40-65 mmHg. In adults, a CPP of less than 40 correlates to poor outcomes. In pediatrics, the true CPP required to maximize outcome is believed to be somewhere along a continuum from 40 to 65 mmHg from infants to adolescents. Current guidelines, however, recommend monitoring systolic blood pressure over mean arterial pressure.

   Clinical indicators of need for fluid resuscitation include tachycardia (with other signs of volume loss and a high index of suspicion), prolonged capillary refill time (>3 seconds), hypotension and loss of central pulses. Remember, hypotension is an extremely late indicator of shock in children.

   Initial pediatric fluid resuscitation includes up to three 20 ml/kg intravenous fluid boluses of crystalloid, isotonic, dextrose-free solutions (0.9% normal saline or lactated Ringer's). If continued resuscitation is required after the initial three boluses, consider packed red blood cells at a volume of 10-15 ml/kg and repeat as needed. It is imperative to evaluate for extracranial injuries to control bleeding. Though it is not likely for children or adults to lose enough blood into the cranial vault to develop shock, infants can bleed enough intracranially to cause circulatory collapse. Hypotension, no matter the cause, must be prevented and promptly treated to reduce morbidity and mortality.

   Hyperosmolar therapy has been only partially evaluated in the pediatric severe TBI population. Currently, both mannitol and hypertonic saline (3% to 23.4% in different studies) are not recommended for prehospital use as brain-targeted therapy; however, general understanding of these treatment options is important for critical care interfacility transport of these patients.

   Overall, although studies of mannitol are limited, it has been used extensively for in-hospital treatment of cerebral edema and has shown positive outcomes in reducing intracranial pressure (ICP). Mannitol rapidly reduces blood viscosity, causing a reflex vasoconstriction of the arterioles by autoregulation. This subsequently decreases cerebral blood volume and intracranial pressure. The effect is rapid and lasts approximately 75 minutes. In addition, the increased serum osmolality caused by mannitol shifts water from brain cells into the intravascular space, causing decreased cellular and cytotoxic edema. This effect has a 15-30-minute onset and lasts up to six hours, but also requires an intact blood brain barrier. The main concern with mannitol administration in severe traumatic brain injury is if the patient does not have an intact blood brain barrier. Mannitol may then shift from the intravascular space into the injured brain regions, which would cause an osmotic shift of fluid from the intravascular space into the brain parenchyma, precipitating more brain edema and increased ICP. Continuous infusion of mannitol rather than typical intermittent boluses is more likely to cause this adverse effect. In addition, mannitol may precipitate hypotension and renal failure. The typical dosing of mannitol is 0.25-1 gm/kg IV bolus, limiting the serum osmolality to no greater than 320 mOsm/L.

   Hypertonic saline has been demonstrated to be effective at lowering ICP in both ICU and operating room settings, but with limited studies. The mechanism of action of hypertonic saline is similar to that of mannitol, with the blood brain barrier being impermeable to both mannitol and sodium (if intact). The theoretical advantage of hypertonic saline is that it can be administered to hemodynamically abnormal patients with impending herniation because it is thought to preserve intravascular volume. In addition, it theoretically restores normal cellular resting membrane potential and cell volume, inhibits inflammation, stimulates atrial naturetic peptide release, and enhances cardiac output. Hypertonic saline, unlike mannitol, is not believed to cause renal failure, but caution is recommended with serum osmolality of greater than 320 mOsm/L due to increased risk of renal insufficiency. Current recommendations state that the serum osmolality should be no greater than 360 mOsm/L. Rebound intracranial hypertension has definitely been documented with administration cessation. Hypertonic saline dosing typically is 3% saline at a rate of 0.1-1 ml/kg/h on a sliding scale with unpublished observations of 1-6 ml/kg boluses used instead at some pediatric trauma centers. The dosing, as well as concentration of hypertonic saline varies substantially throughout trials. As with mannitol, hypertonic saline is not currently recommended for prehospital care as brain-targeted therapy, but may be used during interfacility transfers.

   Steroids, such as methylprednisolone, were once thought to be an effective treatment in reducing cerebral edema and injury. Strong clinical studies have shown that steroid administration in both adult and pediatric TBI does not lower intracranial pressure or improve outcome. Rather, high-dose methylprednisolone in moderate to severe TBI increases mortality. Steroids should not be used in the prehospital setting.

DISABILITY/DEXTROSE

   The Glasgow Coma Scale score has been validated in the prehospital setting to correlate with outcomes in both adult and pediatric TBI patients. The GCS should be evaluated after the ABCs are secured. If an extra provider is available, they may perform the GCS sooner if it does not interfere with or delay the ABCs. If sedation and paralysis are used, the GCS should be evaluated either prior to medication administration or after the medications are metabolized. The standard GCS should be used in all adults and children two years and older. The pediatric GCS, or P-GCS, should be used to evaluate all children younger than two years of age (Figure 5).

   In addition, pupillary response correlates to survival in both general trauma patients and traumatic brain injuries. Asymmetry, also known as anisocoria, or dilated and non-reactive pupils are poor prognostic indicators and, in the proper clinical context, may be a sign of cerebral herniation discussed earlier.

   Always evaluate for orbital injuries during the pupillary exam, as they may cause pupillary changes that do not correlate with true intracranial injury. For example, direct injury to cranial nerve #3 behind the eye can result in abnormal pupillary reaction to light and is not due to a brain injury. In addition, carotid dissection from trauma can lead to Horner's syndrome, causing unequal pupils. This syndrome is characterized by a drooping eyelid with constricted pupil on the affected side and the appearance of a dilated pupil on the opposite side. The dilated pupil will still respond briskly to light.

   A blood glucose or dextrose level should be checked in all traumatic brain injury patients. Administer dextrose in the form of D₂₅W for children and D₁₀W for infants intravenously only if blood glucose levels are low (Figure 6). Administration of dextrose to normoglycemic patients with severe TBI is detrimental.

SECONDARY SURVEY

   All trauma patients require full body exposure to evaluate for other injuries. Pediatric patients especially require increased privacy, support and comfort during this time. Carefully explaining your role to the patient and other family and friends is vital to appropriate care. Remember, too, that pediatric patients have a large surface-to-volume area, so heat loss occurs more rapidly than in adults. It is vital to prevent heat loss during this time.

   The secondary survey is a key component to the care of severe traumatic brain injury patients, along with secondary interventions. Emergent transport of these patients should not be delayed, nor should ABCDE reassessment be compromised. Constantly monitor vital signs, with blood pressure evaluation every five minutes, if possible. Consideration of nonaccidental trauma is a must when evaluating the scene of a pediatric traumatic brain injury. Anderson, et al., in a prospective study of children under two years old admitted with head injuries, found a 24% incidence of nonaccidental trauma as the cause.⁶

TRANSPORT

   Pediatric severe traumatic brain injury outcomes improve when patients are treated at an appropriate facility. Children with severe traumatic brain injuries have an eight times greater risk of death when treated at a non-tertiary hospital. Current guidelines recommend that pediatric patients with mild TBI (GCS 13-15) can be treated at a local ED, with a moderate TBI (GCS 9-12) at a trauma center, and with severe TBI (GCS less than 9) at a pediatric trauma center or adult trauma center with pediatric severe TBI qualifications.

CONCLUSION

   Infants, children and adolescents are at high risk of sustaining a severe traumatic brain injury. The prognosis of the injury, from the time of onset, is poor. One-half of all severe TBI deaths occur within two hours of the incident. With knowledgeable prehospital care of these critically injured children, secondary injury can be prevented to maximize survival and neurological function.

References

1. Carney NA, Chesnut R, Kochanek PM, eds. Guidelines for the acute medical management of severe traumatic brain injuries in infants, children, and adolescents. Ped Crit Care Med J, July 2003.

2. Friess S, et al. An evidence-based approach to severe traumatic brain injury in children. Ped Emerg Med Practice, Dec 2007.

3. Brain Trauma Foundation, American Association of Neurological Surgeons/College of Neurological Surgeons, Joint Section on Neurotrauma and Critical Care. Guidelines for the management of severe head injury. J Neurotrauma, 3rd Ed., 2007.

4. National Association of State EMS Officials, National Association of EMS Educators & National Association of EMTs. Guidelines for the prehospital management of traumatic brain injury, 2nd edition. Supplement to Prehosp Emerg Care 12(1):S37-39, Jan/Mar 2008.

5. Ehrlich PF, et al. Endotracheal intubations in rural pediatric trauma patients. J Pediatr Surg 39(9):1376-1380, 2004.

6. Anderson VA, et al. Identifying factors contributing to child and family outcome 30 months after traumatic brain injury in children. Neurol Neurosurg Psychiatry 75:401-408, Mar 2005.

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   Jeremy DeWall, MD, NREMT-P, is a resident physician practicing emergency medicine at the Medical College of Wisconsin's Department of Emergency Medicine in Milwaukee. He has been a nationally registered paramedic for 10 years. In addition, he works as a flight physician for Flight for Life of Milwaukee.

Figure 1: Pediatric ETT Sizing

Pre-term-6 months: 2.5-4.0 uncuffed

1 year: 4.0-4.5 uncuffed

2+ years old: 16 + (age in years)/4 uncuffed

Depth: 3 x ETT size

No securing around the neck