Pediatric Traumatic Brain Injury

Published on 10/02/2015 by admin

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24 Pediatric Traumatic Brain Injury

Epidemiology

An estimated 615,000 traumatic brain injuries (TBIs) occur each year in patients younger than 19 years; this figure accounts for 26% of pediatric hospitalizations and 15% of all pediatric deaths.1 Children 0 to 4 years of age and older adolescents 15 to 19 years of age are most likely to sustain a TBI. Mild traumatic brain injury (mTBI), or concussion, represents the predominant form of acquired brain injury and accounts for 75% to 90% of all instances.2,3

Pathophysiology

The mechanisms of pediatric TBI are similar to those in adults, with falls being the most common cause. However, child abuse must be considered as an occult mechanism of head injury in preverbal children because abusive head trauma remains the most common cause of traumatic death in infancy. Findings in such patients may be subtle, with nonspecific symptoms (vomiting, fussiness) and no history of trauma. Clinicians must maintain a high index of suspicion for inflicted injury in young children. In older adolescents, sports are a common cause of concussive injury, and return to sports should be addressed in the discharge instructions.

As in adults, the pathophysiology of pediatric head trauma is related to the degree of force. With moderate force, injury can occur to the brain parenchyma, which primarily results in nonoperative lesions, or can involve vascular structures, which typically results in operative lesions.

Patients younger than 2 years are at higher risk for skull fractures, with the most common type being linear fractures. In infants, fractures may occur even after short falls (≤3 to 4 feet). The majority of fractures have an overlying hematoma or swelling; only 15% to 30% are associated with an intracranial injury.4 In general, linear skull fractures heal without incident. Rarely, in children with open fontanelles (<2 years old) and fractures with greater than 3-mm separation, a tear in the dura allows pulsation of cerebrospinal fluid (CSF) or herniated meninges, which impedes fracture healing and extends the fracture over time.5 This may become apparent months to years after the initial injury and usually requires surgical correction. Depressed skull fractures with greater than 5 mm of depression generally require surgical correction. Basilar skull fractures have classic findings on physical examination (raccoon eyes, Battle sign, hemotympanum) and may be associated with cranial nerve palsies (facial palsy, nystagmus, diplopia, and facial numbness), CSF rhinorrhea or otorrhea, and hearing loss.

Best motor response

Medical Decision Making

Clinical decision making has been geared toward reducing the mortality associated with TBI. The greatest improvements in mortality occur when deterioration is prevented in those with minor head injury.

Neuroimaging has been used to identify patients at risk for deterioration following TBI, but clinicians working with pediatric populations must balance the utility of neuroimaging with the risks associated with radiation and sedation (children may require sedation to obtain a computed tomography [CT] scan). Studies suggest that the theoretic risk for fatal brain tumors increases as age at time of intracranial imaging decreases, and even though complications of sedation are rare, many children experience prolonged recovery and delayed side effects.7 Studies have found that approximately 6% of children with minor head injury have abnormal findings on CT and, more important, that less than 1% require neurosurgical intervention.8 When compared with the adult population, pediatric patients are more likely to be seen in the ED following very mild injury, thus further lowering the pretest probability of significant intracranial injury.

Given this tendency, many studies have sought to identify criteria that would guide the use of neuroimaging in pediatric populations. A recent study by the Pediatric Emergency Care Applied Research Network (PECARN) assessed 42,000 pediatric patients to develop a decision rule.9 For children 2 years or younger, they found that patients with abnormal mental status, non–frontal scalp hematoma, loss of consciousness, a severe mechanism of injury, and a palpable skull fracture and those who were not “acting normally” per parent could be accurately predicted to have significant intracranial injury. For patients older than 2 years, they found abnormal mental status, loss of consciousness, significant vomiting, severe mechanism of injury, clinical signs of basilar skull fracture, and severe headache predicted significant intracranial injury (Fig. 24.1). Use of these clinical guidelines would significantly reduce unnecessary intracranial imaging.

Observation is an alternative to neuroimaging in patients with mild injury. A retrospective Canadian study of approximately 17,000 pediatric patients older than 8 years found that delayed deterioration (>6 hours) occurred in no patients with a normal GCS score.10 Pediatric patients are often evaluated several hours after their injury; continued observation within the department or at home would be an acceptable alternative to emergency imaging in low-risk patients.

For patients with mTBI or concussion, emergency department (ED) clinicians in general have not focused on the morbidity associated with this injury and may not recognize their ability to improve patient outcomes. It has been shown that accurate assessment of the severity of the injury and consequent outpatient guidance and management may decrease recovery time, reduce the risk for secondary complications, and improve outcomes. mTBI or concussion can also be challenging to diagnose. Patients with polytrauma or other significant injury may not be screened for the subtle findings associated with concussion, which can result from any blow to the head or an indirect force through the neck or to the body. The immediate symptoms of concussion are the result of trauma-induced alterations in neurologic function and include amnesia (retrograde or anterograde), altered consciousness (loss of consciousness, dazed, stunned, confused), migrainelike symptoms (headache, nausea, photophobia or phonophobia, visual changes, dizziness or balance problems), cognitive symptoms (difficulty concentrating or remembering), and changes in personality. These immediate symptoms are typically short-lived and are associated with a normal findings on physical examination and neuroimaging. Clinicians in the ED are in a unique position to diagnose mTBI and initiate proper management to minimize the adverse outcomes of concussion.

Admission and Discharge

The majority of patients with mTBI or concussion are reassured and discharged home. For these patients, appropriate diagnosis, patient education, and outpatient management may decrease recovery time, reduce the risk for secondary complications, and improve outcomes.11 Pediatric patients with normal neuroimaging findings but persistently abnormal GCS scores, severe vomiting, or unremitting headache should be admitted to the hospital for observation and hydration.

Determining concussion severity and recovery is critical because returning patients to physical activities too soon following concussion can lead to disabling and even life-threatening outcomes such as second impact syndrome, which is the sudden onset of cerebral edema after a second (even minor) concussion. Historically, however, evaluation and management of victims of concussion have been inconsistent. To add to the confusion, more than 25 concussion grading systems exist, each with their own ranking of concussion severity and management recommendations. Unfortunately, these clinical grading systems are not validated and have not allowed clinicians, patients, or families to recognize the spectrum of postconcussive symptoms.

The Centers for Disease Control and Prevention has recently changed its recommendations for acute concussion management from the use of grading scales to use of the Acute Concussion Evaluation (ACE) (see ACE and ACE-Care Plan, available at www.cdc.gov). The ACE is a paper evaluation form that was designed to provide a diagnostic framework for clinicians in the outpatient setting to define concussion and characterize the patient’s symptoms.12 Rather than focus on grading assessments of concussion severity, the ACE provides a standardized tool to aid in identifying mTBI in primary care settings. Unlike grading systems that provide set return-to-play decisions (e.g., those with grade 1 concussion may return to play in 15 minutes), the ACE offers an ACE-Care Plan, a set of best-practice discharge instructions that strongly recommend rest and endorse the “Stepwise Return to Play” (Box 24.1). The ACE-Care Plan also offers extensive information regarding return to school and work to minimize overexertion and improve recovery. The ACE and ACE-Care Plan represent a transition from passive management to active evaluation of concussion and intervention to decrease secondary injury.

Most patients with mTBI will recover within the first 7 to 10 days. In others, postconcussive syndrome will develop, a constellation of neurocognitive symptoms (including headaches, fatigue, sleep problems, changes in personality, photophobia, hyperacusis, dizziness, and deficits in short-term memory and problem solving) that may persist for days to weeks. Athletes who suffer multiple concussions are more likely to be plagued with postconcussive symptoms. School performance may be affected in these children, and some may need specific accommodation plans. Patients at high risk for complications related to mTBI (e.g., athletes, those with previous concussions or personal history of migraines) should be evaluated by a concussion specialist.13

Occasionally, patients with postconcussive syndrome return to the ED for subsequent problems. In patients with waxing and waning postconcussive symptoms or migraine headache, emergency imaging is not necessary except to exclude alternative diagnoses. Postconcussive symptoms respond well to standard migraine treatment (nonsteroidal antiinflammatory drugs, intravenous fluids, antiemetics). These patients should be referred to a concussion specialist for follow-up.

References

1 Sosin DM, Sniezek JE, Thurman DJ. Incidence of mild and moderate brain injury in the United States, 1991. Brain Inj. 1996;10:47–54.

2 Collins MW, Iverson GL, Lovell MR, et al. On-field predictors of neuropsychological and symptom deficit following sports-related concussion. Clin J Sport Med. 2003;13:222–229.

3 Schultz M. Incidence and risk factors for concussion in high school athletes, north carolina, 1996-1999. Am J. Epidemiology. 2004;160:937–944.

4 Greenes DS, Schutzman SA. Infants with isolated skull fracture: what are their clinical characteristics, and do they require hospitalization? Ann Emerg Med. 1997 Sep;30:253–259.

5 Rinehart GC, Pittman T. Growing skull fractures: strategies for repair and reconstruction. J Craniofac Surg. 1998;9:65–72.

6 Holmes JF, Palchak MJ, MacFarlane T, et al. Performance of the pediatric Glasgow Coma Scale in children with blunt head trauma. Acad Emer Med. 2005;12:814–819.

7 Kim PK, Zhu X, Houseknecht E, et al. Effective radiation dose from radiologic studies in pediatric trauma patients. World J Surg. 2005;29:1557–1562.

8 Atabaki SM, Stiell IG, Bazarian JJ, et al. A clinical decision rule for cranial computed tomography in minor pediatric head trauma. Arch Ped Adolescent Med. 2008 May;162:439–445.

9 Kuppermann N, Holmes JF, Dayan PS, et al. Identification of children at very low risk of clinically-important brain injuries after head trauma: a prospective cohort study. Lancet. 2009;374:1160–1170.

10 Hamilton M, Mrazik M, Johnson DW. Incidence of delayed intracranial hemorrhage in children after uncomplicated minor head injuries. Pediatrics. 2010;126:e33–e39.

11 Ponsford J, Willmott C, Rothwell A, et al. Impact of early intervention on outcome after mild traumatic brain injury in children. Pediatrics. 2001;108:1297–1303.

12 Gioia GA, Collins M, Isquith PK. Improving identification and diagnosis of mild traumatic brain injury with evidence: Psychometric support for the acute concussion evaluation. J Head Trauma Rehabil. 2008;23:230–242.

13 McCrory P, Meeuwisse W, Johnston K, et al. Consensus statement on concussion in sport—the 3rd International Conference on Concussion in Sport, held in Zurich, November 2008. J Clin Neurosci. 2009;16:755–763.