A 3-month-old, full-term girl infant with no known past medical history presents to your facility with altered mental status. The mother initially took the patient to her pediatrician the previous day due to concern for fussiness and vomiting. There is no history of fevers, cyanosis, difficulty breathing, abdominal distention, diarrhea, or rash. The patient's mother denies any possibility of trauma or ingestion. At the pediatrician's office, the patient appeared well enough to be discharged home with a diagnosis of a viral illness. After the visit, she had another episode of vomiting and poor feeding prior to going to sleep. In the morning, the mother found the patient unresponsive in her crib, so she called emergency medical services. During transport, the patient is intubated because her Glasgow Coma Scale (GCS) score is 6. After arrival to the emergency department and primary assessment of the patient's airway, breathing, and circulation, a secondary assessment reveals an obtunded infant with fixed pupils (at 4 mm), a full and firm anterior fontanelle, and one bruise on the patient's anterior chest. The patient is stabilized, laboratory results are obtained, and she is quickly taken to radiology for a noncontrast head computed tomography (CT) that demonstrates a large right subdural hematoma, intraparenchymal hemorrhage with an 8-mm midline shift, and diffuse hypoxic ischemic injury (Figure 1). As hypertonic saline is being infused, neurosurgery is notified and the patient is admitted to the pediatric intensive care unit for further management of a severe traumatic brain injury (TBI) from suspected nonaccidental trauma.
Noncontrast computed tomography images of the head demonstrating (A) right subdural hematoma, (B) right to left midline shift, and (C, D) right intraparenchymal hemorrhage. These images should lead to concern for central and tonsillar herniation, cerebral edema, and ischemia.
Pediatric TBI has a significant impact on health care in the United States. An estimated 475,000 TBIs occur among children age 0 to 14 years annually, with the highest rates in children age 0 to 4 years.1 Mild TBI is the most common form of pediatric TBI. When examining global trends, male children suffer higher rates of TBI than female children after age 3 years. The highest rates of head injury show a bimodal distribution in children age 0 to 2 years and adolescents age 15 to 18 years.2 It is estimated the nearly 60,000 TBI-associated hospitalizations in children in the US accounted for more than $2.5 billion in hospital charges in 2006.3 The largest two causes of TBI-related hospitalizations were motor vehicle collisions (38.9%) and falls at (21.2%).3 In younger children, child abuse is an important factor to consider in TBI given that more child abuse deaths occur from head injuries than any other type of injury.4
The brain is a semisolid structure surrounded by cerebrospinal fluid (CSF) and covered by a thin pia-arachnoid membrane as well as a thicker dura membrane within the cranial vault. After closure of the fontanelles in infancy, the cranial vault has a fixed volume made primarily of three components: brain, blood, and CSF. If the volume of one component increases within the cranial vault, then the volume of the other components must subsequently decrease or the intracranial pressure (ICP) will rise (Figure 2).4
The skull is a fixed space that contains brain parenchyma, CSF, and blood. When there is an increase in intracranial pressure due to one component (such as a bleed) in a closed head injury, another component must give way. This can potentially lead to herniation of the brain. CSF, cerebrospinal fluid.
There are two phases of TBI. Primary injury results from direct insult to the brain or by acceleration-deceleration forces at the time of impact. Physical damage occurs by forceful contact of the brain with bony protuberances of the calvarium, bony fracture fragments, or from a penetrating foreign body. Secondary injury is categorized by further neuronal damage in response to the primary insult affecting cells that were not initially injured. Systemic effects such as hypoxia, hypoperfusion, metabolic changes, expanding cerebral edema, hypotension, and hypercapnia can all contribute to this secondary injury. The goal of the clinician is to identify and treat the primary brain injury to limit further neuronal damage by secondary injury.
Cerebral ischemia resulting from impaired perfusion is a common cause of secondary brain injury. Cerebral perfusion pressure (CPP) is the difference between the mean arterial pressure (MAP) of blood flowing to the brain and ICP (ie, CPP = MAP minus ICP).5
With severe TBI, the brain's autoregulation of CPP is lost. Cerebral blood flow depends on this autoregulation to compensate for a decreased MAP or increased ICP, which are common in severe TBI. A decreased CPP can lead to cerebral ischemia.
Brain injuries can be classified as diffuse or focal. Diffuse injury, which includes cerebral edema and diffuse axonal injury, is the type of TBI in children more likely to result in death. Cerebral edema may develop within hours and peak within the first 2 to 4 days after the traumatic event. The most common initial finding on CT is bilateral diffuse cerebral swelling.6 This swelling can cause marked elevations in ICP, so children with significant cerebral edema must be monitored for signs of herniation. Diffuse axonal injury occurs from damage to the white matter tracts of the brain and is often found in children with posttraumatic coma. This may not always be detected on the initial CT scan, but is more evident on subsequent magnetic resonance imaging (MRI).7
There are several types of focal brain injury.8 Brain contusions are often found with blunt head trauma. This may manifest in a “coup” or “countercoup” lesion in which the lesion corresponds with the injured cerebral cortex. Subarachnoid hemorrhage commonly causes a severe “thunder-clap” headache, neck stiffness, and lethargy. An epidural hematoma occurs when blood collects between the skull and the dura. Temporal epidural hemorrhages are commonly associated with injury to the middle meningeal artery. In an epidural hematoma, the patient may have a lucid interval between initial loss of consciousness (LOC) and subsequent deterioration. The CT will often show a lens-shaped fluid collection. Subdural hematomas occur when blood collects between the dura and the arachnoid membranes from shearing of bridging veins. CT may show crescent-shaped fluid collections. Children may present with seizures, evidence of increased intracranial pressure, or nonspecific signs such as vomiting, irritability, low-grade fevers, or a bulging fontanelle in infants. Intracerebral hematomas are less common in children and are often the result of severe focal injury or penetrating trauma yielding a poor prognosis.
Evaluation and Management
The evaluation of any patient with altered mental status starts with a thorough history of precipitating events. Often, the precipitating history may be vague or incomplete, especially if the inciting injury was unwitnessed. Therefore, a broad differential must always be considered. In cases of traumatic head injury, it is helpful to inquire about the mechanism, time of injury, and the evolution of symptoms. Red flags for a serious intracranial process after a head injury include immediate LOC, failure to return to neurological baseline, persistent amnesia, or focal neurological deficits. Vomiting after head injury is more common in children than in adults.9 Isolated vomiting is unlikely to be associated with clinically important brain injury.10 Vomiting along with other signs and symptoms, however, should still prompt further evaluation. Thorough vetting of patient's past medical history is also essential to identify at-risk patients who may be predisposed to more severe injuries. Patients with bleeding disorders, such as hemophilia and von Willebrand disease, are especially at risk for intracranial hemorrhage even with minor head trauma.
A systematic physical examination is also crucial in the initial assessment of a patient after a traumatic head injury. After ensuring adequacy of the airway, breathing, and circulation, a rapid assessment of neurological disability should be performed to screen for signs and symptoms of increased ICP due to edema or bleeding that may warrant prompt neurosurgical intervention. The GCS has consistently been shown to be helpful in categorizing a TBI. A modified pediatric GCS has also been validated for preverbal children.11 Mild, moderate, and severe brain injuries correlate with GCS scores of 14 to 15, 9 to 13, and <9, respectively.12
Although GCS can aid in TBI classification, the patient's clinical status and presenting signs/symptoms should also be considered. Documentation of a complete baseline neurological examination is helpful to objectively track patient improvement or deterioration. Pupillary response should be noted during any evaluation of head trauma. A dilated pupil that does not constrict with light is concerening for an uncal brain herniation and warrants urgent neurosurgical evaluation.
Special attention should be paid to the scalp, where one should look for bruising, swelling, abrasions, and lacerations as well as careful palpation for step-offs and areas of tenderness. Evaluation for signs of a basilar skull fracture includes evaluation for bruising over the mastoid process (Battle's sign), hemotympanum, periorbital bruising (raccoon eyes), CSF rhinorrhea or otorrhea, as well as evaluation for cranial nerve deficits.
For patients thought to have a mild to moderate TBI, implementing a decision tool for head injury, such as the one developed by the Pediatric Emergency Care Applied Research Network (PECARN),13 is useful to guide management. This widely used set of validated prediction rules was developed to identify children at low risk of clinically important TBI (ciTBI).13 Based on these rules, children with a GCS of 14, abnormal mental status, or signs of either basilar or palpable skull fracture have about a 4% risk of ciTBI. Thus, a noncontrast head CT is recommended in these cases. Other isolated findings, including loss of consciousness, vomiting, headache, or nonfrontal scalp hematoma, are less concerning for ciTBI so observation without CT may be appropriate depending on physician experience, parental concern, and symptom progression. If a patient does not present with any of the signs or symptoms mentioned in the decision tool, a head CT is not recommended. External prospective validation found the PECARN tool's sensitivity to be 100%.14
The initial assessment should always begin with stabilizing the patient's airway, breathing, and circulation to minimize hypoxia and hypotension, each of which have been shown to increase mortality in children with TBI.15 If a severe TBI is suspected and emergency pediatric neurosurgical consultation is not immediately available, prompt transfer to a trauma center with pediatric expertise has been shown to result in better outcomes.16 The cervical spine should be immobilized until proper assessment by clinical examination, or radiographic imaging can be performed.
In a child with TBI presenting with altered or worsening mental status, providers should have a high suspicion of increased ICP from ongoing intracranial bleeding and/or brain swelling. Important factors that contribute to an increased ICP include blood pressure, temperature, hypoxia, and acidosis/hypercarbia.17–20 Care must also be taken to avoid or address factors that may raise ICP such as unnecessary stimulation, agitation, vomiting, and pain. The patient's head should be kept midline and the head of the bed elevated between 15 and 30 degrees to improve venous drainage from the head. Seizure prophylaxis with levetiracetam or phenytoin is recommended for the first 7 days after TBI.21,22
If at any time it is determined that the medical facility does not have the resources to appropriately care for TBI, then the patient should be transferred to a trauma center without delay. Upon arrival to a trauma center ED, a primary and secondary survey should assess for and address immediate life-threatening conditions. Intravenous access should be obtained, and baseline laboratory tests should be performed to evaluate for anemia, electrolyte abnormalities, serum glucose, and acid-base status. Intubation is recommended for persistent hypoxia, hypoventilation, or altered mental status resulting in inability to protect the airway.
If the patient continues to show signs of altered mental status and/or impending herniation, hypertonic (3%) saline (HTS) or mannitol can be given as a bolus or continuous infusion to acutely reduce ICP. HTS and mannitol both appear to be effective, but there is no clear consensus of when to use one instead of the other.23
Once stabilized, neuroimaging with an unenhanced CT or rapid MRI of the brain will help to identify the injury and help plan for any necessary neurosurgical intervention. In cases of increased ICP refractory to medical management, surgical decompressive craniotomy may be warranted. Early coordination and communication with neurosurgeons and intensivists is key in developing an effective management strategy.
Patient prognosis is variable depending on the severity of the TBI. Mild TBI (mTBI) frequently results in persistent postconcussive symptoms that can lead to significant morbidity. In pediatric practice, there are well-established guidelines for return to school and sports after mTBI.24,25 Return-to-learn guidelines recommend an individualized approach, which may include academic adjustments or specialized learning plans that minimize worsening of symptoms, as well as a patient-centered team of medical providers, school personnel, and family to assist the student in his or her return to learning. For recovery of longer than 3 weeks, children may benefit from a more detailed assessment by a concussion specialist.24 Return-to-sport guidelines include a six-step process that provides a structured guide to an athlete recovering from mTBI.25 In brief, the protocol begins with no activity, followed by light aerobic exercise, sport-specific exercise, noncontact training drills, full contact practice, and full return to play. Each phase must be achieved without headaches or neurological symptoms before proceeding to the next step.24 The Centers for Disease Control and Prevention recently published guidelines on the diagnosis and management of mTBI in children that are an excellent resource for any medical provider caring for children with TBI.26
There are several important sequelae of mTBI. Second impact syndrome is based on the premise that a second brain injury while still symptomatic can cause cerebral edema and even herniation. There is controversy surrounding this theory and further studies are needed. Chronic traumatic encephalopathy, which is currently receiving much attention in the media, is characterized by symptoms including irritability, impulsivity, attention deficits, as well as problems with memory, executive functioning, and depression. These changes can potentially occur in childhood.27
The primary care physician plays an essential role in preventing TBIs. Providing age and developmentally appropriate anticipatory guidance during wellness visits gives the primary care physician a unique opportunity to assess risk, educate families, and provide injury prevention resources to minimize the risk of childhood and adolescent TBIs. Caring for a colicky infant, proper installation of a car seat, helmet use, and sports safety are just several of many topics that should be discussed. Pediatric providers should also be encouraged to be community advocates, especially promoting safety in youth sports.
When a child or adolescent presents with altered mental status, an astute physician should always consider TBI as part of the differential diagnosis. Properly assessing the severity of a TBI will enable the provider to perform appropriate diagnostic testing and initiate directed treatments. Rapid and thorough decision-making will optimize patient prognosis. Providers in the primary care setting are essential in providing anticipatory guidance. They also frequently manage children with subsequent postconcussive symptoms and provide long-term care for children with significant TBI sequelae.
- Langlois JA, Rutland-Brown W, Thomas KE. The incidence of traumatic brain injury among children in the United States: differences by race. J Head Trauma Rehabil. 2005;20(3):229–238. doi:10.1097/00001199-200505000-00006 [CrossRef]
- Dewan MC, Mummareddy N, Wellons JC, Bonfield CM. Epidemiology of global pediatric traumatic brain injury: qualitative review. World Neurosurg. 2016;91:497–509. doi:. doi:10.1016/j.wneu.2016.03.045 [CrossRef]
- Shi J, Xiang H, Wheeler K, et al. Costs, mortality likelihood and outcomes of hospitalized US children with traumatic brain injuries. Brain Injury. 2009;23(7–8):602–611. doi:. doi:10.1080/02699050903014907 [CrossRef]
- Levitt CJ, Smith WL, Alexander RC. Abusive head trauma. In: Reece RM, ed. Child Abuse: Medical Diagnosis and Management. Philadelphia, PA: Lea & Febiger; 1994:1–22.
- Guilliams K, Wainwright MS. Pathophysiology and management of moderate and severe traumatic brain injury in children. J Child Neurol. 2014;31(1):35–45. doi:. doi:10.1177/0883073814562626 [CrossRef]
- Bruce DA, Alavi A, Bilaniuk L, Dolinskas C, Obrist W, Uzzell B. Diffuse cerebral swelling following head injuries in children: the syndrome of “malignant brain edema.”J Neurosurg. 1981;54(2):170–178. doi:10.3171/jns.1981.54.2.0170 [CrossRef]
- Tasker RC. Changes in white matter late after severe traumatic brain injury in childhood. Dev Neurosci. 2006;28(4–5):302–308. doi:. doi:10.1159/000094156 [CrossRef]
- Schutzman SA, Mannix R. Injury: head. In: Shaw KN, Bachur RG, eds. Fleisher & Ludwig's Textbook of Pediatric Emergency Medicine. 7th ed. Philadelphia, PA: Wolters Kluwer; 2010:247–253.
- Brown FD, Brown J, Beattie TF. Why do children vomit after minor head injury?Emerg Med J. 2000;17:268–271. doi:10.1136/emj.17.4.268 [CrossRef]
- Dayan PS, Holmes JF, Atabaki S, et al. Traumatic Brain Injury Study Group of the Pediatric Emergency Care Applied Research Network (PECARN). Association of traumatic brain injuries with vomiting in children with blunt head trauma. Ann Emerg Med. 2014;63(6):657–665. doi:. doi:10.1016/j.annemergmed.2014.01.009 [CrossRef]
- Borgialli DA, Mahajan P, Hoyle JD Jr, et al. Performance of the pediatric Glasgow Coma Scale score in the evaluation of children with blunt head trauma. Acad Emerg Med. 2016;23:878–884. doi:. doi:10.1111/acem.13014 [CrossRef]
- Schutzman SA, Greenes DS. Pediatric minor head trauma. Ann Emerg Med. 2001;37(1):65–74. doi:10.1067/mem.2001.109440 [CrossRef]
- 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(9696):1160–1170. doi:. doi:10.1016/S0140-6736(09)61558-0 [CrossRef]
- Lorton F, Poullaouec C, Legallais E, et al. Validation of the PECARN clinical decision rule for children with minor head trauma: a French multicenter prospective study. Scand J Trauma Resusc Emerg Med. 2016;24:98. doi:. doi:10.1186/s13049-016-0287-3 [CrossRef]
- Adelson PD. Chapter 3. Prehospital airway management. Pediatr Crit Care Med. 2003;4(suppl 3):S9–S11. doi:10.1097/00130478-200307001-00004 [CrossRef]
- Potoka DA, Schall LC, Gardner MJ, Stafford PW, Peitzman AB, Ford HR. Impact of pediatric trauma centers on mortality in a statewide system. J Trauma. 2000;49:237–245. doi:10.1097/00005373-200008000-00009 [CrossRef]
- American Heart Association. Part 12: pediatric advanced life support. Web-based integrated 2015 & 2018 American Heart Association guidelines for CPR and ECC. https://eccguidelines.heart.org/index.php/circulation/cpr-ecc-guidelines-2/part-12-pediatric-advanced-life-support/. Accessed on April 19, 2019.
- Carney N, Totten AM, O'Reilly C, et al. Guidelines for the management of severe traumatic brain injury, fourth edition. Neurosurgery. 2017;80(1):6–15. doi:10.1227/NEU.0000000000001432 [CrossRef].
- Hardcastle N, Benzon HA, Vavilala MS. Update on the 2012 guidelines for the management of pediatric traumatic brain injury – information for the anesthesiologist. Paediatr Anaesth. 2014;24(7):703–710. doi:. doi:10.1111/pan.12415 [CrossRef]
- Kochanek PM, Carney N, Adelson PD, et al. Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents—second edition. Pediatr Crit Care Med. 2012;13(1):S1–S82. doi:. doi:10.1097/PCC.0b013e318259ee85 [CrossRef]
- Chang BS, Lowenstein DH. Practice parameter: antiepileptic drug prophylaxis in severe traumatic brain injury: report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2003;60(1):10–16. doi:10.1212/01.WNL.0000031432.05543.14 [CrossRef]
- Nita DA, Hahn CD. Levetiracetam for pediatric posttraumatic seizure prophylaxis. Pediatr Neurol Brief. 2016;30(3):18. doi:. doi:10.15844/pedneurbriefs-30-3-1 [CrossRef]
- Boone MD, Oren-Grinberg A, Robinson TM, Chen CC, Kasper EM. Mannitol or hypertonic saline in the setting of traumatic brain injury: what have we learned?Surg Neurol Int. 2015;6:177. doi:. doi:10.4103/2152-7806.170248 [CrossRef]
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- May KH, Marshall DL, Burns TG, Popoli DM, Polikandriotis JA. Pediatric sports specific return to play guidelines following concussion. Int J Sports Phys Ther. 2014;9(2):242–255.
- Lumba-Brown A, Yeates KO, Sarmiento K, et al. Centers for Disease Control and Prevention guideline on the diagnosis and management of mild traumatic brain injury among children. JAMA Pedriatr. 2018;172(11):e182853. doi:. doi:10.1001/jamapediatrics.2018.2853 [CrossRef]
- Rose SC, Weber KD, Collen JB, Heyer GL. The diagnosis and management of concussion in children and adolescents. Pediatr Neurol. 2015;53(2):108–118. doi:. doi:10.1016/j.pediatrneurol.2015.04.003 [CrossRef]