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Evidence-Based Assessment of Severe Pediatric Traumatic Brain Injury and Emergent Neurocritical Care
Evidence-Based Assessment of Severe Pediatric Traumatic Brain Injury and Emergent Neurocritical Care Angela Lumba-Brown, MD, FAAP,* and Jose Pineda, MD, MSCI† Pediatric traumatic brain injury accounts for approximately 474,000 emergency department visits, 37,000 hospitalizations, and 3,000 deaths in children 14 years and younger annually in the United States. Acute neurocritical care in children has advanced with specialized pediatric trauma centers and emergency medical services. This article reviews pediatricspecific diagnosis, management, and medical decision making related to the neurocritical care of severe traumatic brain injury. Semin Pediatr Neurol 21:275-283 C 2014 Published by Elsevier Inc.
Opening Vignette A 12-year-old boy is brought to the emergency department (ED) via emergency medical services (EMS) after transport from the scene of a motor vehicle collision (MVC). The EMS crew tells you that the patient was found restrained in the rear passenger-side seat. The patient had loss of consciousness at the scene for an unknown duration of time and is now “waking up.” En route, the crew was unable to obtain intravenous (IV) access but did put the patient in a cervical spineimmobilization collar and on a backboard. On initial evaluation, he is moaning and will not open his eyes, and withdraws from pain. His respiratory rate is 10 breaths per minute, heart rate is 62 beats per minute, and blood pressure is 135/90 mm Hg. He has no external signs of injury except for a large parieto-occipital cephalohematoma. Issues to address include the following: Rapid identification of Cushing’s triad Rapid identification of airway instability Vascular access in the pediatric patient with trauma Need to perform a complete primary and secondary survey
Introduction Half a million emergency department (ED) visits for traumatic brain injury (TBI) are made annually by children 14 years and younger.1 Pediatric TBI is a leading cause of From the *Division of Pediatric Emergency Medicine, Washington University School of Medicine, St. Louis, MO. †Pediatric Neurocritical Care, Washington University School of Medicine, St. Louis, MO. Address reprint requests to Angela Lumba-Brown, MD, FAAP, Pediatric Emergency Medicine, Washington University School of Medicine, St. Louis, MO. E-mail: [email protected]
1071-9091/14/$-see front matter & 2014 Published by Elsevier Inc. http://dx.doi.org/10.1016/j.spen.2014.11.001
morbidity and mortality in the United States and costs $1 billion per year.2 Quality acute care and the coordination of multidisciplinary care involving trauma surgery, neurosurgery, radiology, emergency medicine, critical care medicine, and neurology are crucial to patient outcomes. The Centers for Disease Control studied the Brain Trauma Foundation's in-hospital guidelines for the treatment of adults with severe TBI and found that widespread adoption could result in a 50% decrease in mortality.3 A 2012 study published in the Lancet Neurology found that TBI outcomes in children can be improved with best practice guidelines in the pediatric intensive care unit (PICU).4 The Brain Trauma Foundation has also published extensive in-hospital pediatric guidelines for severe TBI.5 These guidelines are not specific to the PICU; for example, early insults such as hypotension, hypothermia, and hypoxemia cause secondary injury and should be immediately addressed. Severe TBI in children is clinically defined symptomatically by a Glasgow Coma Scale (GCS) Score less than 9 or a GCS of 9-12 with impending decompensation.
Critical Appraisal of the Literature The body of literature related to severe TBI and neurocritical care in adults is extensive, and pediatric care is often extrapolated. However, the direct applicability to the pediatric patient is uncertain. This review focuses mainly on pediatric-specific research and identifies gaps in knowledge. This literature review was launched with Ovid MEDLINE and PubMed searches for articles on pediatric severe TBI from 1999-2014. Keywords included the following: pediatric severe traumatic brain injury, pediatric TBI, and 275
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276 pediatric neurocritical care. These articles were limited to all infants and all children 0-18 years old. This search yielded 1757 articles. Literature search was supplanted with review of adult severe TBI topics as well. In total, 65 predominantly pediatric studies are included as the basis for the discussion in this publication with the oldest published in 1984. They comprise a growing body of literature of clinical trials, multicenter observational studies, meta-analysis, and reviews that have resulted in multiple practice guidelines for pediatric neurocritical care. In 2012, the Brain Trauma Foundation created evidencebased guidelines for the in-hospital care of pediatric patients with brain injury.5
Epidemiology The Centers for Disease Control has called TBI a public health problem in children.6 TBI accounts for 40% of injury-related pediatric deaths.6 Between 1995 and 2001, pediatric TBI caused almost 3,000 deaths and 473,947 ED visits in the US per year.6 In 2000, the pediatric TBIassociated hospitalization rate was 70 cases per 100,000 children. Adolescents, 15-17 years of age, had the highest hospitalization percentage.2
positioning and skilled technique with intubation to secure a stable airway in a child with severe TBI. Children's cooperation and communication skills are minimal in younger age groups representing a challenge in history taking and in assessing their GCS and any new neurologic deficits.
Pathophysiology Injuries to the brain can be classified as primary or secondary injury. Primary brain injury refers to the effect of the initial insult. Secondary injury is caused by a complex biomechanical cascade of events that may be worsened by insults to hemodynamic and metabolic status (Fig.). There are 2 general types of brain injury: diffuse and focal. Head injury can result in a combination of the 2 and manifest from both primary and secondary injuries. Diffuse head injury includes diffuse axonal injury, which is defined by the National Institute of Neurological Disorders and Stroke on radiologic imaging as small and scattered lesions representing widespread injury to white matter axons in more than one lobe or hemisphere.7 Focal injuries include contusions and intracranial hemorrhage: subdural, epidural, and subarachnoid.
Differential Diagnosis
Etiology Causes of TBI in children vary by age. Falls are the most common cause of TBI in young children.6 Motor vehicle accidents, other accidents, and sports injuries are the most common in older children and adolescents. Motor vehicle accidents cause the majority of TBI-related deaths in children.1 Nonaccidental trauma (NAT) is a serious concern in infants and in any child with unexplainable head injury, which is further discussed in the section Special Circumstances. As compared with adults, children's heads are larger in proportion to their bodies. Developing coordination skills in younger children and risk-taking behaviors further increase children's risk for head injury and subsequent potential TBI. A child can have significant blood loss into cephalohematomas or bleeding scalp laceration. An infant's open anterior fontanel may permit enlarging space-occupying lesions such as hematoma without clear physical decompensation. A child's occiput is larger proportionately than an adult's is. A child's airway is more anterior than an adult's is, requiring
The differential diagnosis of severe TBI is clinically focused on causes of altered mental status. Generally the pediatric patient with severe TBI has a known and often witnessed history of trauma. However, patients with NAT or unwitnessed trauma may present with altered mental status, for which there are many differential diagnoses (Table 1).
Prehospital Care and Interfacility Transport Emergency medical services (EMS) systems in the United States are directed on a state-by-state level. Currently, there are no national prehospital protocols for the management of pediatric TBI. However, the National Association of State EMS Officials is currently developing recommended EMS guidelines. The Brain Trauma Foundation developed Guidelines for the Prehospital Management of Severe TBI; however, these are not pediatric specific.8
Hypoxemia Secondary Injury
Primary Injury Hypotension
Hypoglycemia Figure Pathophysiological mechanisms of brain injury. (Color version of figure is available online.)
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Table 1 The Differential Diagnosis of Severe TBI* Differential Diagnosis
Physical Examination
Focused Diagnostic Considerations
Epilepsy Shock
Seizure, altered mental status Tachycardia, hypotension, delayed capillary refill, altered mental status Metabolic acidosis, toxidromic symptoms, altered mental status Fever, headache, meningismus, irritability Neurologic deficit Altered mental status, headache, vomiting Fever, tachycardia, other infectious symptoms Altered mental status, vomiting, headache, discoordination Altered mental status, seizures Altered mental status, seizures
EEG Mean arterial pressure, creatinine, transaminases, lactate VBG and electrolytes, EKG
Toxic ingestion Meningitis/encephalitis Stroke Hydrocephalus Sepsis Severe concussion Hypoglycemia Hyponatremia
CSF analysis with culture CT head, MRI brain, angiography CT head CBC, blood culture, urine culture, CSF culture Observation versus imaging Serum blood glucose Serum electrolytes
CSF, cerebrospinal fluid; CBC, complete blood count; EEG, electroencephalogram; EKG, electrocardiogram; MRI, magnetic resonance imaging; CT head, head computed tomography; VBG, venous blood gas. *In the absence of witnessed trauma, the differential diagnosis for severe TBI includes pathologies that present with altered mental status.
Initial assessment by EMS providers begins with evaluating and supporting a patient's airway, breathing, and circulation. Often in cases of head injury, prehospital providers maintain cervical spine (c-spine) immobilization and transport the patient on a backboard. This is especially important in the patient with altered mental status and an unclear neurologic examination. Emergency medical technicians-Intermediate and paramedics are certified to obtain intravenous (IV) access and perform advanced airway techniques in the field.9 Some ambulance crews can use end-tidal CO2 (ETCO2) monitoring. The American College of Surgeons Committee on Trauma, in collaboration with the American Academy of Pediatrics, the American College of Emergency Physicians, and other academic institutions, has developed and updated recommended pediatric equipment lists for ambulances.10 Approved EMS agencies are allowed by the Office of Emergency Medical Services and Trauma to approve paramedic administration of sedative medications for use with intubation. Often this is in conjunction with online medical control, in which case communication of neurologic examination before medication administration will be useful to the evaluating medical team. Pediatric patients with trauma are transferred to tertiary care facilities including children's hospitals. Transferring and accepting hospitals operate under the Emergency Medical Treatment and Labor Act, which provides that if a hospital does not have the capability to treat the emergency medical condition, the patient must be transferred to the nearest capable hospital. The transferring physician must perform a medical screening examination and ensure that the patient is reasonably stable for transfer. In the case of a child with severe TBI, this requires at minimum IV access and ensuring a stable airway. Although obtaining brain imaging is not mandatory before the transfer of a child with suspected severe TBI, head computed tomography (CT) imaging is fast and provides valuable information to the receiving facility.
The transferring physician certifies that the medical benefits outweigh the risks of transfer, and this physician generally acts as medical control for that patient during transfer. Exclusion to this medical control would be in the case of tertiary hospital transport teams who provide transport from the referring hospital to the receiving hospital. These transport teams may be staffed with a combination of paramedics, nurse practitioners, and physicians who are generally under the medical control of the receiving hospital. Children with suspected severe TBI must be accompanied by a life support service that has experience with pediatric critical care, including intubation and medication administration, and should be transferred via the fastest means possible including ambulance, helicopter, or fixed-wing aircraft.
Continued Vignette You suspected severe TBI in the 12-year-old male patient with altered mental status following MVC and with a parieto-occipital cephalohematoma. You correctly identified his GCS as 7: eye opening score of 1, verbal score of 2, and motor score of 4. You immediately placed the patient on oxygen and elevated the head of his bed while establishing 2 large-bore IV access sites. His hypertension and bradycardia with altered mental status and irregular respirations are consistent with Cushing triad, and you are concerned for impending cerebral herniation. You instruct your trauma team to monitor the patient's ETCO2 and to transiently hyperventilate the patient to maintain ETCO2 at 3035 mm Hg while your pharmacist prepares 5 mL/kg of 3% hypertonic saline. His respiratory rate remains 10-12 breaths per minute, heart rate is 60s-70s, and blood pressure is 135/90 mm Hg. You correctly determine that this patient will require a secure airway. As you are preparing to intubate, the nurse recycles the blood pressure, and you note it is 93/66 mm Hg. Issues to address include the following:
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278 Management of hypotension in the patient with severe TBI Contraindications to types of osmolar therapy in the hypotensive patient Neurosurgical consultation
The Evaluation The evaluation begins with immediate assessment of the patient's airway, breathing, and circulatory status as well as GCS and other indicators of disability. Critical care begins immediately and is best provided with access to a multidisciplinary team of pediatric emergency medicine physicians, trauma surgeons, neurosurgeons, anesthesiologists, pharmacists, and radiology technicians. The priority of care is patient stabilization with diagnosis of TBI and any coexisting conditions. The next step is coordination with surgical subspecialties and critical care medicine to evaluate if the patient is a candidate for operative repair or continued medical management in the PICU. Predictors of poor outcome in children with severe TBI include age-appropriate systolic blood pressure (SBP) o75th percentile, hypothermia, and NAT.11
Physical Examination Important physical findings in the patient with suspected severe TBI include the following: vital signs assessment, pediatric GCS and neurologic examination, evidence of skull fractures including basilar skull fractures, presence of cephalohematoma, or skull abnormality such as penetrating wounds. Initial physical examination includes primary and secondary trauma survey with evaluation of other distracting injuries or injuries that may suggest NAT.
Airway Stability The pediatric patient with a history of significant head trauma is at risk for c-spine injury and airway compromise owing to direct trauma, potential increased intracranial pressure (ICP) with brainstem compression, and loss of protective airway mechanism such as gag reflex.12 A pediatric patient with altered mental status requires cervical collar immobilization and a secure airway with endotracheal intubation using a cuffed endotracheal tube. The airway is maintained with jaw thrust for intubation, and c-spine precautions are maintained manually while ccollar is temporarily removed during the procedure. Pediatric patients who are awake and alert at the time of arrival may allow for a complete c-spine examination supported by negative x-ray results to confirm c-spine clearance. Patients with TBI are maintained in cervical collars until they are alert and awake without distracting injuries or in the case of an obtunded patient, until clearance by neurosurgery following a normal c-spine MRI finding.13 c-spine xrays are helpful in identifying bony injuries. However, x-rays and CT scans of the c-spine are not definitive in identifying
c-spine injury in young children with neck pain or altered mental status because they may have spinal cord injury without radiographic abnormality owing to the elasticity of the pediatric spine and ligaments.14
Adequate Exchange of Oxygenation Breathing and the adequate exchange of oxygen in patients with TBI affect metabolic demand and cerebral blood flow. Hypoxia causes increased metabolic demands and increased cerebral blood flow.15 The patients are generally oxygenated with 100% O2 to maintain saturations above 92%.
Effective Circulation Hypotension after severe TBI increases the risk of secondary brain injury owing to reduced perfusion to viable neural tissue.16,17 Pediatric hypotension in a patient with trauma is defined as blood pressure o5th percentile for age that lasts longer than 5 minutes.17 The Brain Trauma Foundation further defined hypotension in the pediatric patient with trauma by age.18 Odds of good outcome are improved when maintaining SBP 475th percentile for age.11 The maintenance of effective circulation is crucial to the patient with TBI in which autoregulation of cerebral perfusion pressure (CPP) may be impaired.19 As compared with adults, children will often preserve their blood pressure and may initially only manifest hypovolemia as tachycardia. Tachycardia in the child with suspected severe TBI requires immediate evaluation.
Disability The standard GCS has been validated for use in children 3 years of age and older, and the Pediatric GCS should be used for infants through 2 years of age18,20 (Table 2). Initial scores should be obtained before the administration of sedatives, narcotics, and paralytics. Assessment should be repeated for any improvement or deterioration in the child's mental status. Pupil examination is a predictive adjunct to the GCS score. In a study of 51,000 patients with trauma, 95% of patients with unequal or fixed pupils had TBI.21 A complete neurologic examination assesses for motor strength, sensation, tone, and cranial nerve deficit as well as deep tendon reflexes, allowing for localization of brain and spinal cord injury.
Exposure Pediatric patients with suspected TBI undergo complete primary and secondary trauma evaluations. This includes completely undressing and rolling the patient to assess for injuries to the back of the body including spinal tenderness or step-offs. Once complete, except when contraindicated by hyperthermia, the patient is covered with warmed blankets. Hypothermia is defined as temperature o35.01C and hyperthermia is defined as temperature 437.91C. There is debate about induced hypothermia in children
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Table 2 The Glasgow Coma Scale51,52 Response
Glasgow Coma Scale
Pediatric Glasgow Coma Scale
Eye Opening
Spontaneous To speech To pain None Oriented Confused Inappropriate words Incomprehensible sounds None Follows commands Localizes pain Withdraws to pain Abnormal flexion Abnormal extension None
Spontaneous To speech To pain None Coos, babbles, age-appropriate speech Irritable, cries Cries to pain Moans to pain None Normal spontaneous movements Withdraws to touch Withdraws to pain Abnormal flexion Abnormal extension None
Verbal Response
Motor Response
with acute TBI. Currently this is a topic under research across the country, but it is not standard of care to induce hypothermia in the child.22
History of Presenting Illness Children with severe TBI are often transported to the ED via EMS, and guardians/witnesses to the injury are not immediately available. In such cases, history of injury may be obtained by EMS while other medical personnel contact an appropriate witness and guardian. Important points in the history include if the child is not acting like his or her usual self, protracted vomiting, worsening symptoms, and severe headache.23 Mechanism of injury may raise suspicion for other injuries in the altered patient such as c-spine injury and intra-abdominal injury or NAT. History of acute drug intoxication may be another explanation of altered mental status or hemodynamic changes. Timing of injury is important because it is extremely rare for a child with severe TBI to present with symptoms greater than 6 hours later. A retrospective cohort showed that 2 of 18,000 children presenting to the ED with minor head injury had delayed deterioration after 6 hours.24 A delay in seeking medical care for a head injury in a child should alert the clinician to the possibility of NAT or medical neglect.25
Past Medical History Important past medical history include the following. Drug allergies History of coagulopathy History of previous head injuries History of previous head imaging and their results History of developmental delay History of seizures
Score 4 3 2 1 5 4 3 2 1 6 5 4 3 2 1
Diagnostic Studies Imaging The gold standard diagnostic study used for identifying acute TBI is head CT, and as many as 50% of the children assessed for head trauma in North American EDs undergo this test.26 Head CT is the best neuroimaging modality to evaluate for emergent traumatic intracranial pathology because it is fast (obtained in minutes) and is accurate for intracranial haemorrhage and skull fracture. Emergent head CT should be obtained in any child suspected of severe TBI. However, there are risks of radiation exposure with CT to consider if indications for imaging are unclear. CT imaging carries a risk of subsequent malignancy extrapolated as 1 fatal cancer per 1000-5000 pediatric head CT examinations based on the data from Japan's atomic bomb survivors.27,28 Children are 10 times more radiosensitive than adults, and radiologists in nonchildren's hospitals should consider that the principles of employing radiation amounts “as low as reasonably achievable” for imaging because a 200mAs adult-protocolled head CT scan delivers twice the amount of radiation (1.8-3.8 mSv) as a similar pediatricprotocolled 100-mAs scan (0.9-1.9 mSv).29,30 Severe TBI has been associated with contusion, hematoma, diffuse axonal injury, cerebral edema, penetrating injury, pneumocephalus, subarachnoid hemorrhage, cistern alterations, midline shift, and fractures.31,32 Brain magnetic resonance imaging is currently not commonly obtained emergently owing to availability and time to obtain imaging.
Complete Blood Count The complete blood count will evaluate for anemia and thrombocytopenia. Additionally, the white blood cell count may assist in the evaluation of differential diagnosis in obtunded patients in which history of trauma is unknown.
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Complete Metabolic Profile Baseline serum electrolytes including sodium and glucose are valuable to the neurocritical care of pediatric patients with TBI. Hyperglycemia is a predictor of poor outcome in children with TBI, and an electrolyte abnormality can be readily addressed in the acute setting.33
Coagulopathy Profile Coagulopathy is defined by an international normalized ratio of 41.5 or the platelet count was o100,000.11 Disseminated intravascular coagulation is a predictor of poor outcome in children with TBI.33
ICP Monitoring CPP is calculated as the mean arterial pressure minus ICP. It is unclear whether the cause of secondary brain injury is primarily owing to increased ICP or decreased CPP. Secondary brain injury occurs owing to cerebral herniation with focal ischemic injury and brainstem compression. Intracranial hypertension is defined as an ICP 420 mm Hg and is associated with poor neurologic outcome and death.34,35 In 2007, Dean et al surveyed 194 pediatric intensivists and neurosurgeons and found that 90% agree with CPP monitoring. Diffuse cerebral swelling on CT is 75% predictive of increased ICP.36 Lack of spontaneous motor function may be an indication of intracranial hypertension.37 Several studies have found increased ICP in children with severe TBI. Adult studies show a benefit in reducing ICP. The Brain Trauma Foundation recommends ICP monitoring in pediatric patients with severe TBI.5
Stabilization And Treatment Rapid Sequence Intubation Stabilization of the neurocritical patient begins with securing a stable airway with endotracheal intubation. In unconscious patients and patients with low GCS scores with hemodynamic instability, the use of sedative and paralytic medications may not be necessary to secure a stable airway and will prevent risks associated with the administration of these medications. In all other patients, rapid sequence intubation (RSI) uses analgesia, sedatives, and paralytics to create optimal conditions to perform emergent intubation. Many of the sedative medications for RSI, such as midazolam and propofol, can cause detrimental side effects such as hypotension. Paralytics prevent neurologic examination if their effects are long lasting as with vecuronium. Currently, succinylcholine and rocuronium are paralytic agents used most frequently in pediatric patients with TBI. Previously, it was thought that succinylcholine caused increases in ICP; however, lack of definitive evidence has contributed to widespread use in patients with TBI.38 The body of evidence supporting lidocaine as an adjuvant to RSI in children with potential increased ICP is lacking, and risk for arrhythmia associated with this agent
should be heavily considered against the lack of clear scientific evidence for benefit.39
Ventilation Pediatric patients requiring assisted ventilation via bag and mask or via endotracheal intubation benefit from ETCO2 monitoring to ensure hyperventilation and hypoventilation do not occur. Hyperventilation (PCO2 o35 mm Hg) decreases cerebral blood flow and can contribute to cerebral ischemia.40 Transient hyperventilation with an ETCO2 goal of 30-35 mm Hg can be performed in the pediatric patient with signs of increased ICP and herniation and in the patient with increased ICP refractory to osmotic agents.5 In 2007, the Journal of Trauma published a prospective study on ventilation in adult patients with trauma.41 Those with ventilation reflected by CO2 30-35 mm Hg were less likely to die than those outside this range. Patients with hypercapnia had greater injury severity scores.
Fluid Resuscitation Fluid resuscitation in children begins with isotonic fluid boluses of 20 mL/kg with consideration given to the need for blood products in a patient who sustained significant blood loss. Hypotension in the pediatric patient with TBI is a predictor of poor outcome.42 In fact, supranormal blood pressures or SBPs above the 75th percentile for age are associated with improved outcome.11,43 Vasopressors may be used as an adjunct in the maintenance of SBP.
Intracranial Hypertension and Hyperosmolar Agents A GCS less than 9 indicates severe TBI with an increased risk of intracranial hypertension.34 Low scores on specifically the motor component of the GCS may indicate intracranial hypertension.44 Intracranial hypertension is more prevalent in children with severe TBI who do not demonstrate spontaneous motor function.37 The presence of diffuse cerebral swelling on head CT greatly increases the likelihood of intracranial hypertension.36 Successful control of intracranial hypertension improves clinical outcomes.45 This can be achieved by sedation, hyperosmolar therapy, and paralysis by the ED physician. Neurosurgical intervention may include ventriculostomy and surgical decompression. Hyperosmolar therapy to reduce increased ICP can be achieved with mannitol (1 g/kg) or hypertonic saline (510 mL/kg) in the pediatric population. Both mannitol and sodium have a low penetration across the blood-brain barrier creating an osmotic gradient effect in circulating blood. This osmotic effect requires an intact blood-brain barrier.
Antiepileptics Seizures increase brain metabolic demands and can cause increased ICP. Prophylaxis with antiepileptics reduces the incidence of posttraumatic seizures in children with TBI.46
Evidence-based assessment of severe pediatric TBI and emergent neurocritical care The most commonly used medications are phenytoin and levetiracetam.47
Disposition Pediatric patients with severe TBI are admitted to the operating room at neurosurgical discretion or a PICU with neurocritical care capabilities.
Special Circumstances Preverbal Children and Evaluating for NAT Children younger than 2 years represent a special group of patients with head injury in which the threshold to evaluate with imaging is lower despite higher risks of radiation. Inherently, these young patients lack verbal skills to relate historical aspects of the injury as well as symptoms, making communication, and evaluation by the clinician difficult. A 2009 Pediatric Emergency Care Applied Research Network study successfully evaluated more than 10,000 children less than 2 years of age to derive and validate prediction rules in children at very low risk of clinically important TBI after head trauma.9 The prediction rule recommends CT for children younger than 2 years with a GCS of 14 or less, other signs of altered mental status, or palpable skull fracture. The Pediatric Emergency Care Applied Research Network study excluded patients in whom TBI may have been sustained by NAT. Importantly, children younger than 2 years are at higher risk for NAT. In circumstances where NAT is suspected owing to delay in seeking care, or the injury does not match the stated mechanism of injury or the child's developmental stage, a head CT and skeletal survey are warranted, and laboratory work assessing for intraabdominal injury should be considered. Often victims of NAT will present with little history or no history of trauma. The treating clinician must maintain a level of suspicion in children with altered mental status and proactively evaluate for TBI.
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severe TBI should be managed according to the neurocritical care parameters discussed in this article.
Controversies The hypotensive patient with severe TBI requires judicious use of sedative agent in rapid sequence induction. The risks of sedation in patients who have very low GCS scores and hypotension may outweigh the benefits, and decisions for sedation in these cases should be made individually. However, for patients with some level of awareness, sedation is necessary. Using a sedative that exacerbates hypotension or causes even transient hypotension in the pediatric patient with TBI risks secondary injury. Etomidate and ketamine are the 2 commonly used sedatives that preserve blood pressure. Both have potential adverse effects, which must be considered. Ketamine has been used for sedation since the 1970s. Historically, it has not been used in patients with TBI because several case series and observational studies in the 1970s suggested its use was associated with increased ICP. Since then, several studies, including randomized controlled trials, have refuted this idea and even proposed that ketamine may improve increased ICP. Rapid sequence induction with etomidate has been shown to worsen adrenal insufficiency as compared with ketamine in patients with severe TBI. Approximately 50% of patients with moderate-severe TBI sedated with a single dose of etomidate will have transient adrenal insufficiency. The effects of this insufficiency are not currently known.
Conclusion Pediatric severe TBI is the leading cause of accidental deaths in children. Excellent emergent management of these children improves their chance at better outcomes. Insults such as hypoxia and hypotension can be minimized with appropriate emergent care, including increased ICP. All patients with severe TBI are admitted for neurocritical care to the operating room or the PICU.
Second Impact Syndrome Second impact syndrome has been described exclusively in children who suffered a mild TBI followed by a second blow to the head before concussive symptoms resolved resulting in severe injury. All reported cases have been in patients younger than 20 years.48,49 The metabolic derangements of mild TBI results in a “situation of metabolic vulnerability, to the point that if another, equally mild injury were to occur, the two mild TBIs would show the biochemical equivalence of a severe TBI.” This hypothesis suggests the pathophysiology of second impact syndrome.50 The hypothesized pathology of second impact syndrome involves cerebral vascular congestion with progression to diffuse cerebral swelling and death. Regardless of etiology, any child with
Vignette Conclusion Your 12-year-old male patient with GCS of 7 became hypotensive in the ED with signs of increased ICP. You correctly initiated fluid resuscitation with 20 mL/kg of normal saline as well as a 5 mL/kg infusion of 3% hypertonic saline. The patient's blood pressure of 93/66 mm Hg improved to 110/80 mm Hg, and he was successfully intubated. The patient remained unconscious but hemodynamically stable on evaluation by the neurosurgical team. He was transported for head CT, which revealed a large epidural hematoma. The neurosurgical team emergently admitted the patient to the operating room for evacuation.
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References 1. Faul M, Xu L, Wald MM, et al: Traumatic Brain Injury in the United States: Emergency Department Visits, Hospitalizations, and DeathsAtlanta, GA, Centers for Disease Control and Prevention, National Center for Injury Prevention and Control, 2010 2. Schneier AJ, Shields BJ, Hostetler SG, et al: Incidence of pediatric traumatic brain injury and associated hospital resource utilization in the United States. Pediatrics 118:483, 2006 3. Faul M, Wald MM, Rutland-Brown W, Sullivent EE, Sattin RW: Using a cost-benefit analysis to estimate outcomes of a clinical treatment guideline: testing the Brain Trauma Foundation guidelines for the treatment of severe traumatic brain injury. J Trauma 63:1271-1278, 2007 4. Pineda JA, Leonard JR, Mazotas IG, et al: Effect of implementation of a paediatric neurocritical care programme on outcomes after severe traumatic brain injury: A retrospective cohort study. Lancet Neurol 12:45-52, 2013 5. 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 13:S1-82, 2012 (suppl 1) 6. Langlois JA, Rutland-Brown W, Thomas KE (eds.), Traumatic Brain Injury in the United States: Emergency Department Visits, Hospitalizations, and Deaths. Atlanta, GA, Centers for Disease Control and Prevention, National Center for Injury Prevention and Control, 2006 7. Duhaime AC, Gean AD, Haacke EM, et al: Common data elements in radiologic imaging of traumatic brain injury. Arch Phys Med Rehabil 91:1661-1666, 2010 8. Brain Trauma Foundation. Guidelines for prehospital management of traumatic brain injury (ed 2). http://www.braintraumafoundation.org 9. National EMS scope of practice model. The National Highway Traffic Safety Administration. http://www.ems.gov/EducationStandards.htm 10. American Academy of Pediatrics, American College of Emergency Physicians, American College of Surgeons Committee on Trauma, et al: Equipment for ground ambulances. Prehosp Emerg Care 18:92-97, 2014 11. Vavilala MS, Bowen A, Lam AM, et al: Blood pressure and outcome after severe pediatric traumatic brain injury. J Trauma 55:1039-1044, 2003 12. 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 36:1107, 2001 13. Leonard JC, Kuppermann N, Olsen C, et al: Factors associated with cervical spine injury in children after blunt trauma. Ann Emerg Med 58:145-155, 2011 14. Mahajan P, Jaffe DM, Olsen CS, et al: Spinal cord injury without radiologic abnormality in children imaged with magnetic resonance imaging. J Trauma Acute Care Surg 75:843-847, 2013 15. Xu F, Liu P, Pascual JM, et al: Effect of hypoxia and hyperoxia on cerebral blood flow, blood oxygenation, and oxidative metabolism. J Cereb Blood Flow Metab 32:1909-1918, 2012 16. Chesnut RM, Marshall LF, Klauber MR, et al: The role of secondary brain injury in determining outcome from severe head injury. J Trauma 34:216-222, 1993 17. Kokoska ER, Smith GS, Pittman T, et al: Early hypotension worsens neurological outcome in pediatric patients with moderately severe head trauma. J Pediatr Surg 33:333-338, 1998 18. Badjatia N, Carney N, Crocco TJ, et al: Guidelines for prehospital management of traumatic brain injury 2nd edition. Prehosp Emerg Care 12:S1-52, 2008 (suppl 1) 19. 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 28:348, 2006 20. Morray JP, Tyler DC, Jones TK, et al: Coma scale for use in brain inured children. Crit Care Med 12:1018-1020, 1984 21. Hoffmann M, Lefering R, Rueger JM, et al: Pupil evaluation in addition to Glasgow Coma Scale components in prediction of traumatic brain injury and mortality. Br J Surg 99:122-130, 2012 (suppl 1)
A. Lumba-Brown and J. Pineda 22. Adelson PD, Wisniewski SR, Beca J, et al: Comparison of hypothermia and normothermia after severe traumatic brain injury in children (Cool Kids): A phase 3, randomised controlled trial. Lancet Neurol 12:546-553, 2013 23. 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 374:1160-1170, 2009 24. Hamilton M: Incidence of delayed intracranial hemorrhage in children after uncomplicated minor head injuries. Pediatrics 126:e40-e45, 2010 25. Krugman RD: Fatal child abuse: Analysis of 24 cases. Pediatrician 12:68-72, 1983 26. Marr A, Coronado V: Central nervous system injury surveillance data submission standards—2002. Atlanta, GA, CDC, National Center for Injury Prevention and Control, 2004 27. Brody AS, Frush DP, Huda W, et al: Radiation risk to children from computed tomography. Pediatrics 120:677-682, 2007 28. Frush DP, Donnelly LF, Rosen NS: Computed tomography and radiation risks: What pediatric health care providers should know. Pediatrics 112:951-957, 2003 29. Slovis TL: Children, computed tomography radiation dose, and the As Low As Reasonably Achievable (ALARA) concept. Pediatrics 112:971-972, 2003 30. Radiation risks and pediatric computed tomography (CT): A guide for healthcare providers. Bethesda, MD, National Cancer Institute, 2002. http://www.cancer.gov/cancertopics/causes/radiation/radiation-riskspediatric-CT 31. Levi L, Guilburd JN, Linn S, et al: The association between skull fracture, intracranial pathology and outcome in pediatric head injury. Br J Neurosurg 5:617-625, 1991 32. Stein SC, Spettell C, Young G, et al: Delayed and progressive brain injury in closed- head trauma: Radiological demonstration. Neurosurgery 32:25-30, 1993 33. Chiaretti A, Piastra M, Pulitanò S, et al: Prognostic factors and outcome of children with severe head injury: An 8-year experience. Childs Nerv Syst 18:129, 2002 34. Barzilay Z, Augarten A, Sagy M, et al: Variables affecting outcome from severe brain injury in children. Intensive Care Med 14:417-421, 1988 35. Cruz J, Nakayama P, Imamura JH, et al: Cerebral extraction of oxygen and intracranial hypertension in severe, acute, pediatric brain trauma: Preliminary novel management strategies. Neurosurgery 50:774-779, 2002 36. Shapiro K, Marmarou A: Clinical applications of the pressure–volume index in treatment of pediatric head injuries. J Neurosurg 56:819-825, 1982 37. Bruce DA, et al: Pathophysiology, treatment and outcome following severe head injury in children. Childs Brain 5:174-191, 1979 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 78:469, 1994 39. Vaillancourt C, Kapur AK: Opposition to the use of lidocaine in rapid sequence intubation. Ann Emerg Med 49:86-87, 2007 40. 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 26:200, 1997 41. Warner KJ, Cuschieri J, Copass MK, et al: The impact of prehospital ventilation on outcome after severe traumatic brain injury. J Trauma 62:1330-1336, 2007 42. Samant UB 4th, Mack CD, Koepsell T, et al: Time of hypotension and discharge outcome in children with severe traumatic brain injury. J Neurotrauma 25:495, 2008 43. White JR, Farukhi Z, Bull C, et al: Predictors of outcome in severely head-injured children. Crit Care Med 29:534, 2001 44. Heuer GG, Smith MJ, Elliott JP, et al: Relationship between intracranial pressure and other clinical variables in patients with aneurysmal subarachnoid hemorrhage. J Neurosurg 101:408-416, 2004 45. Jagannathan J, Okonkwo DO, Yeoh HK, et al: Long-term outcomes and prognostic factors in pediatric patients with severe traumatic brain injury and elevated intracranial pressure. J Neurosurg Pediatr 2:240-249, 2008
Evidence-based assessment of severe pediatric TBI and emergent neurocritical care 46. Lewis RJ, Yee L, Inkelis SH, et al: Clinical predictors of post-traumatic seizures in children with head trauma. Ann Emerg Med 22:1114, 1993 47. Jones KE, Puccio AM, Harshman KJ, et al: Levetiracetam versus phenytoin for seizure prophylaxis in severe traumatic brain injury. Neurosurg Focus 25:E3, 2008 48. Mueller FO: Catastrophic head injuries in high school and collegiate sports. J Athl Train 36:312-315, 2001 49. Saunders RL, Harbaugh RE: The second impact in catastrophic contact sports head trauma. J Am Med Assoc 252:538-539, 1984
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50. Mild Traumatic Brain Injury Committee of the Head Injury Interdisciplinary Special Interest Group of the American Congress of Rehabilitation Medicine. J Head Trauma Rehabil 8:86-87, 1993 51. Teasdale G, Jennett B: Assessment of coma and impaired consciousness. A practical scale. Lancet 2:81, 1974 52. Holmes JF, Palchak MJ, MacFarlane T, Kuppermann N: Performance of the pediatric Glasgow coma scale in children with blunt head trauma. Acad Emerg Med 12:814, 2005
Opening Vignette A 12-year-old boy is brought to the emergency department (ED) via emergency medical services (EMS) after transport from the scene of a motor vehicle collision (MVC). The EMS crew tells you that the patient was found restrained in the rear passenger-side seat. The patient had loss of consciousness at the scene for an unknown duration of time and is now “waking up.” En route, the crew was unable to obtain intravenous (IV) access but did put the patient in a cervical spineimmobilization collar and on a backboard. On initial evaluation, he is moaning and will not open his eyes, and withdraws from pain. His respiratory rate is 10 breaths per minute, heart rate is 62 beats per minute, and blood pressure is 135/90 mm Hg. He has no external signs of injury except for a large parieto-occipital cephalohematoma. Issues to address include the following: Rapid identification of Cushing’s triad Rapid identification of airway instability Vascular access in the pediatric patient with trauma Need to perform a complete primary and secondary survey
Introduction Half a million emergency department (ED) visits for traumatic brain injury (TBI) are made annually by children 14 years and younger.1 Pediatric TBI is a leading cause of From the *Division of Pediatric Emergency Medicine, Washington University School of Medicine, St. Louis, MO. †Pediatric Neurocritical Care, Washington University School of Medicine, St. Louis, MO. Address reprint requests to Angela Lumba-Brown, MD, FAAP, Pediatric Emergency Medicine, Washington University School of Medicine, St. Louis, MO. E-mail: [email protected]
1071-9091/14/$-see front matter & 2014 Published by Elsevier Inc. http://dx.doi.org/10.1016/j.spen.2014.11.001
morbidity and mortality in the United States and costs $1 billion per year.2 Quality acute care and the coordination of multidisciplinary care involving trauma surgery, neurosurgery, radiology, emergency medicine, critical care medicine, and neurology are crucial to patient outcomes. The Centers for Disease Control studied the Brain Trauma Foundation's in-hospital guidelines for the treatment of adults with severe TBI and found that widespread adoption could result in a 50% decrease in mortality.3 A 2012 study published in the Lancet Neurology found that TBI outcomes in children can be improved with best practice guidelines in the pediatric intensive care unit (PICU).4 The Brain Trauma Foundation has also published extensive in-hospital pediatric guidelines for severe TBI.5 These guidelines are not specific to the PICU; for example, early insults such as hypotension, hypothermia, and hypoxemia cause secondary injury and should be immediately addressed. Severe TBI in children is clinically defined symptomatically by a Glasgow Coma Scale (GCS) Score less than 9 or a GCS of 9-12 with impending decompensation.
Critical Appraisal of the Literature The body of literature related to severe TBI and neurocritical care in adults is extensive, and pediatric care is often extrapolated. However, the direct applicability to the pediatric patient is uncertain. This review focuses mainly on pediatric-specific research and identifies gaps in knowledge. This literature review was launched with Ovid MEDLINE and PubMed searches for articles on pediatric severe TBI from 1999-2014. Keywords included the following: pediatric severe traumatic brain injury, pediatric TBI, and 275
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276 pediatric neurocritical care. These articles were limited to all infants and all children 0-18 years old. This search yielded 1757 articles. Literature search was supplanted with review of adult severe TBI topics as well. In total, 65 predominantly pediatric studies are included as the basis for the discussion in this publication with the oldest published in 1984. They comprise a growing body of literature of clinical trials, multicenter observational studies, meta-analysis, and reviews that have resulted in multiple practice guidelines for pediatric neurocritical care. In 2012, the Brain Trauma Foundation created evidencebased guidelines for the in-hospital care of pediatric patients with brain injury.5
Epidemiology The Centers for Disease Control has called TBI a public health problem in children.6 TBI accounts for 40% of injury-related pediatric deaths.6 Between 1995 and 2001, pediatric TBI caused almost 3,000 deaths and 473,947 ED visits in the US per year.6 In 2000, the pediatric TBIassociated hospitalization rate was 70 cases per 100,000 children. Adolescents, 15-17 years of age, had the highest hospitalization percentage.2
positioning and skilled technique with intubation to secure a stable airway in a child with severe TBI. Children's cooperation and communication skills are minimal in younger age groups representing a challenge in history taking and in assessing their GCS and any new neurologic deficits.
Pathophysiology Injuries to the brain can be classified as primary or secondary injury. Primary brain injury refers to the effect of the initial insult. Secondary injury is caused by a complex biomechanical cascade of events that may be worsened by insults to hemodynamic and metabolic status (Fig.). There are 2 general types of brain injury: diffuse and focal. Head injury can result in a combination of the 2 and manifest from both primary and secondary injuries. Diffuse head injury includes diffuse axonal injury, which is defined by the National Institute of Neurological Disorders and Stroke on radiologic imaging as small and scattered lesions representing widespread injury to white matter axons in more than one lobe or hemisphere.7 Focal injuries include contusions and intracranial hemorrhage: subdural, epidural, and subarachnoid.
Differential Diagnosis
Etiology Causes of TBI in children vary by age. Falls are the most common cause of TBI in young children.6 Motor vehicle accidents, other accidents, and sports injuries are the most common in older children and adolescents. Motor vehicle accidents cause the majority of TBI-related deaths in children.1 Nonaccidental trauma (NAT) is a serious concern in infants and in any child with unexplainable head injury, which is further discussed in the section Special Circumstances. As compared with adults, children's heads are larger in proportion to their bodies. Developing coordination skills in younger children and risk-taking behaviors further increase children's risk for head injury and subsequent potential TBI. A child can have significant blood loss into cephalohematomas or bleeding scalp laceration. An infant's open anterior fontanel may permit enlarging space-occupying lesions such as hematoma without clear physical decompensation. A child's occiput is larger proportionately than an adult's is. A child's airway is more anterior than an adult's is, requiring
The differential diagnosis of severe TBI is clinically focused on causes of altered mental status. Generally the pediatric patient with severe TBI has a known and often witnessed history of trauma. However, patients with NAT or unwitnessed trauma may present with altered mental status, for which there are many differential diagnoses (Table 1).
Prehospital Care and Interfacility Transport Emergency medical services (EMS) systems in the United States are directed on a state-by-state level. Currently, there are no national prehospital protocols for the management of pediatric TBI. However, the National Association of State EMS Officials is currently developing recommended EMS guidelines. The Brain Trauma Foundation developed Guidelines for the Prehospital Management of Severe TBI; however, these are not pediatric specific.8
Hypoxemia Secondary Injury
Primary Injury Hypotension
Hypoglycemia Figure Pathophysiological mechanisms of brain injury. (Color version of figure is available online.)
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Table 1 The Differential Diagnosis of Severe TBI* Differential Diagnosis
Physical Examination
Focused Diagnostic Considerations
Epilepsy Shock
Seizure, altered mental status Tachycardia, hypotension, delayed capillary refill, altered mental status Metabolic acidosis, toxidromic symptoms, altered mental status Fever, headache, meningismus, irritability Neurologic deficit Altered mental status, headache, vomiting Fever, tachycardia, other infectious symptoms Altered mental status, vomiting, headache, discoordination Altered mental status, seizures Altered mental status, seizures
EEG Mean arterial pressure, creatinine, transaminases, lactate VBG and electrolytes, EKG
Toxic ingestion Meningitis/encephalitis Stroke Hydrocephalus Sepsis Severe concussion Hypoglycemia Hyponatremia
CSF analysis with culture CT head, MRI brain, angiography CT head CBC, blood culture, urine culture, CSF culture Observation versus imaging Serum blood glucose Serum electrolytes
CSF, cerebrospinal fluid; CBC, complete blood count; EEG, electroencephalogram; EKG, electrocardiogram; MRI, magnetic resonance imaging; CT head, head computed tomography; VBG, venous blood gas. *In the absence of witnessed trauma, the differential diagnosis for severe TBI includes pathologies that present with altered mental status.
Initial assessment by EMS providers begins with evaluating and supporting a patient's airway, breathing, and circulation. Often in cases of head injury, prehospital providers maintain cervical spine (c-spine) immobilization and transport the patient on a backboard. This is especially important in the patient with altered mental status and an unclear neurologic examination. Emergency medical technicians-Intermediate and paramedics are certified to obtain intravenous (IV) access and perform advanced airway techniques in the field.9 Some ambulance crews can use end-tidal CO2 (ETCO2) monitoring. The American College of Surgeons Committee on Trauma, in collaboration with the American Academy of Pediatrics, the American College of Emergency Physicians, and other academic institutions, has developed and updated recommended pediatric equipment lists for ambulances.10 Approved EMS agencies are allowed by the Office of Emergency Medical Services and Trauma to approve paramedic administration of sedative medications for use with intubation. Often this is in conjunction with online medical control, in which case communication of neurologic examination before medication administration will be useful to the evaluating medical team. Pediatric patients with trauma are transferred to tertiary care facilities including children's hospitals. Transferring and accepting hospitals operate under the Emergency Medical Treatment and Labor Act, which provides that if a hospital does not have the capability to treat the emergency medical condition, the patient must be transferred to the nearest capable hospital. The transferring physician must perform a medical screening examination and ensure that the patient is reasonably stable for transfer. In the case of a child with severe TBI, this requires at minimum IV access and ensuring a stable airway. Although obtaining brain imaging is not mandatory before the transfer of a child with suspected severe TBI, head computed tomography (CT) imaging is fast and provides valuable information to the receiving facility.
The transferring physician certifies that the medical benefits outweigh the risks of transfer, and this physician generally acts as medical control for that patient during transfer. Exclusion to this medical control would be in the case of tertiary hospital transport teams who provide transport from the referring hospital to the receiving hospital. These transport teams may be staffed with a combination of paramedics, nurse practitioners, and physicians who are generally under the medical control of the receiving hospital. Children with suspected severe TBI must be accompanied by a life support service that has experience with pediatric critical care, including intubation and medication administration, and should be transferred via the fastest means possible including ambulance, helicopter, or fixed-wing aircraft.
Continued Vignette You suspected severe TBI in the 12-year-old male patient with altered mental status following MVC and with a parieto-occipital cephalohematoma. You correctly identified his GCS as 7: eye opening score of 1, verbal score of 2, and motor score of 4. You immediately placed the patient on oxygen and elevated the head of his bed while establishing 2 large-bore IV access sites. His hypertension and bradycardia with altered mental status and irregular respirations are consistent with Cushing triad, and you are concerned for impending cerebral herniation. You instruct your trauma team to monitor the patient's ETCO2 and to transiently hyperventilate the patient to maintain ETCO2 at 3035 mm Hg while your pharmacist prepares 5 mL/kg of 3% hypertonic saline. His respiratory rate remains 10-12 breaths per minute, heart rate is 60s-70s, and blood pressure is 135/90 mm Hg. You correctly determine that this patient will require a secure airway. As you are preparing to intubate, the nurse recycles the blood pressure, and you note it is 93/66 mm Hg. Issues to address include the following:
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278 Management of hypotension in the patient with severe TBI Contraindications to types of osmolar therapy in the hypotensive patient Neurosurgical consultation
The Evaluation The evaluation begins with immediate assessment of the patient's airway, breathing, and circulatory status as well as GCS and other indicators of disability. Critical care begins immediately and is best provided with access to a multidisciplinary team of pediatric emergency medicine physicians, trauma surgeons, neurosurgeons, anesthesiologists, pharmacists, and radiology technicians. The priority of care is patient stabilization with diagnosis of TBI and any coexisting conditions. The next step is coordination with surgical subspecialties and critical care medicine to evaluate if the patient is a candidate for operative repair or continued medical management in the PICU. Predictors of poor outcome in children with severe TBI include age-appropriate systolic blood pressure (SBP) o75th percentile, hypothermia, and NAT.11
Physical Examination Important physical findings in the patient with suspected severe TBI include the following: vital signs assessment, pediatric GCS and neurologic examination, evidence of skull fractures including basilar skull fractures, presence of cephalohematoma, or skull abnormality such as penetrating wounds. Initial physical examination includes primary and secondary trauma survey with evaluation of other distracting injuries or injuries that may suggest NAT.
Airway Stability The pediatric patient with a history of significant head trauma is at risk for c-spine injury and airway compromise owing to direct trauma, potential increased intracranial pressure (ICP) with brainstem compression, and loss of protective airway mechanism such as gag reflex.12 A pediatric patient with altered mental status requires cervical collar immobilization and a secure airway with endotracheal intubation using a cuffed endotracheal tube. The airway is maintained with jaw thrust for intubation, and c-spine precautions are maintained manually while ccollar is temporarily removed during the procedure. Pediatric patients who are awake and alert at the time of arrival may allow for a complete c-spine examination supported by negative x-ray results to confirm c-spine clearance. Patients with TBI are maintained in cervical collars until they are alert and awake without distracting injuries or in the case of an obtunded patient, until clearance by neurosurgery following a normal c-spine MRI finding.13 c-spine xrays are helpful in identifying bony injuries. However, x-rays and CT scans of the c-spine are not definitive in identifying
c-spine injury in young children with neck pain or altered mental status because they may have spinal cord injury without radiographic abnormality owing to the elasticity of the pediatric spine and ligaments.14
Adequate Exchange of Oxygenation Breathing and the adequate exchange of oxygen in patients with TBI affect metabolic demand and cerebral blood flow. Hypoxia causes increased metabolic demands and increased cerebral blood flow.15 The patients are generally oxygenated with 100% O2 to maintain saturations above 92%.
Effective Circulation Hypotension after severe TBI increases the risk of secondary brain injury owing to reduced perfusion to viable neural tissue.16,17 Pediatric hypotension in a patient with trauma is defined as blood pressure o5th percentile for age that lasts longer than 5 minutes.17 The Brain Trauma Foundation further defined hypotension in the pediatric patient with trauma by age.18 Odds of good outcome are improved when maintaining SBP 475th percentile for age.11 The maintenance of effective circulation is crucial to the patient with TBI in which autoregulation of cerebral perfusion pressure (CPP) may be impaired.19 As compared with adults, children will often preserve their blood pressure and may initially only manifest hypovolemia as tachycardia. Tachycardia in the child with suspected severe TBI requires immediate evaluation.
Disability The standard GCS has been validated for use in children 3 years of age and older, and the Pediatric GCS should be used for infants through 2 years of age18,20 (Table 2). Initial scores should be obtained before the administration of sedatives, narcotics, and paralytics. Assessment should be repeated for any improvement or deterioration in the child's mental status. Pupil examination is a predictive adjunct to the GCS score. In a study of 51,000 patients with trauma, 95% of patients with unequal or fixed pupils had TBI.21 A complete neurologic examination assesses for motor strength, sensation, tone, and cranial nerve deficit as well as deep tendon reflexes, allowing for localization of brain and spinal cord injury.
Exposure Pediatric patients with suspected TBI undergo complete primary and secondary trauma evaluations. This includes completely undressing and rolling the patient to assess for injuries to the back of the body including spinal tenderness or step-offs. Once complete, except when contraindicated by hyperthermia, the patient is covered with warmed blankets. Hypothermia is defined as temperature o35.01C and hyperthermia is defined as temperature 437.91C. There is debate about induced hypothermia in children
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Table 2 The Glasgow Coma Scale51,52 Response
Glasgow Coma Scale
Pediatric Glasgow Coma Scale
Eye Opening
Spontaneous To speech To pain None Oriented Confused Inappropriate words Incomprehensible sounds None Follows commands Localizes pain Withdraws to pain Abnormal flexion Abnormal extension None
Spontaneous To speech To pain None Coos, babbles, age-appropriate speech Irritable, cries Cries to pain Moans to pain None Normal spontaneous movements Withdraws to touch Withdraws to pain Abnormal flexion Abnormal extension None
Verbal Response
Motor Response
with acute TBI. Currently this is a topic under research across the country, but it is not standard of care to induce hypothermia in the child.22
History of Presenting Illness Children with severe TBI are often transported to the ED via EMS, and guardians/witnesses to the injury are not immediately available. In such cases, history of injury may be obtained by EMS while other medical personnel contact an appropriate witness and guardian. Important points in the history include if the child is not acting like his or her usual self, protracted vomiting, worsening symptoms, and severe headache.23 Mechanism of injury may raise suspicion for other injuries in the altered patient such as c-spine injury and intra-abdominal injury or NAT. History of acute drug intoxication may be another explanation of altered mental status or hemodynamic changes. Timing of injury is important because it is extremely rare for a child with severe TBI to present with symptoms greater than 6 hours later. A retrospective cohort showed that 2 of 18,000 children presenting to the ED with minor head injury had delayed deterioration after 6 hours.24 A delay in seeking medical care for a head injury in a child should alert the clinician to the possibility of NAT or medical neglect.25
Past Medical History Important past medical history include the following. Drug allergies History of coagulopathy History of previous head injuries History of previous head imaging and their results History of developmental delay History of seizures
Score 4 3 2 1 5 4 3 2 1 6 5 4 3 2 1
Diagnostic Studies Imaging The gold standard diagnostic study used for identifying acute TBI is head CT, and as many as 50% of the children assessed for head trauma in North American EDs undergo this test.26 Head CT is the best neuroimaging modality to evaluate for emergent traumatic intracranial pathology because it is fast (obtained in minutes) and is accurate for intracranial haemorrhage and skull fracture. Emergent head CT should be obtained in any child suspected of severe TBI. However, there are risks of radiation exposure with CT to consider if indications for imaging are unclear. CT imaging carries a risk of subsequent malignancy extrapolated as 1 fatal cancer per 1000-5000 pediatric head CT examinations based on the data from Japan's atomic bomb survivors.27,28 Children are 10 times more radiosensitive than adults, and radiologists in nonchildren's hospitals should consider that the principles of employing radiation amounts “as low as reasonably achievable” for imaging because a 200mAs adult-protocolled head CT scan delivers twice the amount of radiation (1.8-3.8 mSv) as a similar pediatricprotocolled 100-mAs scan (0.9-1.9 mSv).29,30 Severe TBI has been associated with contusion, hematoma, diffuse axonal injury, cerebral edema, penetrating injury, pneumocephalus, subarachnoid hemorrhage, cistern alterations, midline shift, and fractures.31,32 Brain magnetic resonance imaging is currently not commonly obtained emergently owing to availability and time to obtain imaging.
Complete Blood Count The complete blood count will evaluate for anemia and thrombocytopenia. Additionally, the white blood cell count may assist in the evaluation of differential diagnosis in obtunded patients in which history of trauma is unknown.
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Complete Metabolic Profile Baseline serum electrolytes including sodium and glucose are valuable to the neurocritical care of pediatric patients with TBI. Hyperglycemia is a predictor of poor outcome in children with TBI, and an electrolyte abnormality can be readily addressed in the acute setting.33
Coagulopathy Profile Coagulopathy is defined by an international normalized ratio of 41.5 or the platelet count was o100,000.11 Disseminated intravascular coagulation is a predictor of poor outcome in children with TBI.33
ICP Monitoring CPP is calculated as the mean arterial pressure minus ICP. It is unclear whether the cause of secondary brain injury is primarily owing to increased ICP or decreased CPP. Secondary brain injury occurs owing to cerebral herniation with focal ischemic injury and brainstem compression. Intracranial hypertension is defined as an ICP 420 mm Hg and is associated with poor neurologic outcome and death.34,35 In 2007, Dean et al surveyed 194 pediatric intensivists and neurosurgeons and found that 90% agree with CPP monitoring. Diffuse cerebral swelling on CT is 75% predictive of increased ICP.36 Lack of spontaneous motor function may be an indication of intracranial hypertension.37 Several studies have found increased ICP in children with severe TBI. Adult studies show a benefit in reducing ICP. The Brain Trauma Foundation recommends ICP monitoring in pediatric patients with severe TBI.5
Stabilization And Treatment Rapid Sequence Intubation Stabilization of the neurocritical patient begins with securing a stable airway with endotracheal intubation. In unconscious patients and patients with low GCS scores with hemodynamic instability, the use of sedative and paralytic medications may not be necessary to secure a stable airway and will prevent risks associated with the administration of these medications. In all other patients, rapid sequence intubation (RSI) uses analgesia, sedatives, and paralytics to create optimal conditions to perform emergent intubation. Many of the sedative medications for RSI, such as midazolam and propofol, can cause detrimental side effects such as hypotension. Paralytics prevent neurologic examination if their effects are long lasting as with vecuronium. Currently, succinylcholine and rocuronium are paralytic agents used most frequently in pediatric patients with TBI. Previously, it was thought that succinylcholine caused increases in ICP; however, lack of definitive evidence has contributed to widespread use in patients with TBI.38 The body of evidence supporting lidocaine as an adjuvant to RSI in children with potential increased ICP is lacking, and risk for arrhythmia associated with this agent
should be heavily considered against the lack of clear scientific evidence for benefit.39
Ventilation Pediatric patients requiring assisted ventilation via bag and mask or via endotracheal intubation benefit from ETCO2 monitoring to ensure hyperventilation and hypoventilation do not occur. Hyperventilation (PCO2 o35 mm Hg) decreases cerebral blood flow and can contribute to cerebral ischemia.40 Transient hyperventilation with an ETCO2 goal of 30-35 mm Hg can be performed in the pediatric patient with signs of increased ICP and herniation and in the patient with increased ICP refractory to osmotic agents.5 In 2007, the Journal of Trauma published a prospective study on ventilation in adult patients with trauma.41 Those with ventilation reflected by CO2 30-35 mm Hg were less likely to die than those outside this range. Patients with hypercapnia had greater injury severity scores.
Fluid Resuscitation Fluid resuscitation in children begins with isotonic fluid boluses of 20 mL/kg with consideration given to the need for blood products in a patient who sustained significant blood loss. Hypotension in the pediatric patient with TBI is a predictor of poor outcome.42 In fact, supranormal blood pressures or SBPs above the 75th percentile for age are associated with improved outcome.11,43 Vasopressors may be used as an adjunct in the maintenance of SBP.
Intracranial Hypertension and Hyperosmolar Agents A GCS less than 9 indicates severe TBI with an increased risk of intracranial hypertension.34 Low scores on specifically the motor component of the GCS may indicate intracranial hypertension.44 Intracranial hypertension is more prevalent in children with severe TBI who do not demonstrate spontaneous motor function.37 The presence of diffuse cerebral swelling on head CT greatly increases the likelihood of intracranial hypertension.36 Successful control of intracranial hypertension improves clinical outcomes.45 This can be achieved by sedation, hyperosmolar therapy, and paralysis by the ED physician. Neurosurgical intervention may include ventriculostomy and surgical decompression. Hyperosmolar therapy to reduce increased ICP can be achieved with mannitol (1 g/kg) or hypertonic saline (510 mL/kg) in the pediatric population. Both mannitol and sodium have a low penetration across the blood-brain barrier creating an osmotic gradient effect in circulating blood. This osmotic effect requires an intact blood-brain barrier.
Antiepileptics Seizures increase brain metabolic demands and can cause increased ICP. Prophylaxis with antiepileptics reduces the incidence of posttraumatic seizures in children with TBI.46
Evidence-based assessment of severe pediatric TBI and emergent neurocritical care The most commonly used medications are phenytoin and levetiracetam.47
Disposition Pediatric patients with severe TBI are admitted to the operating room at neurosurgical discretion or a PICU with neurocritical care capabilities.
Special Circumstances Preverbal Children and Evaluating for NAT Children younger than 2 years represent a special group of patients with head injury in which the threshold to evaluate with imaging is lower despite higher risks of radiation. Inherently, these young patients lack verbal skills to relate historical aspects of the injury as well as symptoms, making communication, and evaluation by the clinician difficult. A 2009 Pediatric Emergency Care Applied Research Network study successfully evaluated more than 10,000 children less than 2 years of age to derive and validate prediction rules in children at very low risk of clinically important TBI after head trauma.9 The prediction rule recommends CT for children younger than 2 years with a GCS of 14 or less, other signs of altered mental status, or palpable skull fracture. The Pediatric Emergency Care Applied Research Network study excluded patients in whom TBI may have been sustained by NAT. Importantly, children younger than 2 years are at higher risk for NAT. In circumstances where NAT is suspected owing to delay in seeking care, or the injury does not match the stated mechanism of injury or the child's developmental stage, a head CT and skeletal survey are warranted, and laboratory work assessing for intraabdominal injury should be considered. Often victims of NAT will present with little history or no history of trauma. The treating clinician must maintain a level of suspicion in children with altered mental status and proactively evaluate for TBI.
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severe TBI should be managed according to the neurocritical care parameters discussed in this article.
Controversies The hypotensive patient with severe TBI requires judicious use of sedative agent in rapid sequence induction. The risks of sedation in patients who have very low GCS scores and hypotension may outweigh the benefits, and decisions for sedation in these cases should be made individually. However, for patients with some level of awareness, sedation is necessary. Using a sedative that exacerbates hypotension or causes even transient hypotension in the pediatric patient with TBI risks secondary injury. Etomidate and ketamine are the 2 commonly used sedatives that preserve blood pressure. Both have potential adverse effects, which must be considered. Ketamine has been used for sedation since the 1970s. Historically, it has not been used in patients with TBI because several case series and observational studies in the 1970s suggested its use was associated with increased ICP. Since then, several studies, including randomized controlled trials, have refuted this idea and even proposed that ketamine may improve increased ICP. Rapid sequence induction with etomidate has been shown to worsen adrenal insufficiency as compared with ketamine in patients with severe TBI. Approximately 50% of patients with moderate-severe TBI sedated with a single dose of etomidate will have transient adrenal insufficiency. The effects of this insufficiency are not currently known.
Conclusion Pediatric severe TBI is the leading cause of accidental deaths in children. Excellent emergent management of these children improves their chance at better outcomes. Insults such as hypoxia and hypotension can be minimized with appropriate emergent care, including increased ICP. All patients with severe TBI are admitted for neurocritical care to the operating room or the PICU.
Second Impact Syndrome Second impact syndrome has been described exclusively in children who suffered a mild TBI followed by a second blow to the head before concussive symptoms resolved resulting in severe injury. All reported cases have been in patients younger than 20 years.48,49 The metabolic derangements of mild TBI results in a “situation of metabolic vulnerability, to the point that if another, equally mild injury were to occur, the two mild TBIs would show the biochemical equivalence of a severe TBI.” This hypothesis suggests the pathophysiology of second impact syndrome.50 The hypothesized pathology of second impact syndrome involves cerebral vascular congestion with progression to diffuse cerebral swelling and death. Regardless of etiology, any child with
Vignette Conclusion Your 12-year-old male patient with GCS of 7 became hypotensive in the ED with signs of increased ICP. You correctly initiated fluid resuscitation with 20 mL/kg of normal saline as well as a 5 mL/kg infusion of 3% hypertonic saline. The patient's blood pressure of 93/66 mm Hg improved to 110/80 mm Hg, and he was successfully intubated. The patient remained unconscious but hemodynamically stable on evaluation by the neurosurgical team. He was transported for head CT, which revealed a large epidural hematoma. The neurosurgical team emergently admitted the patient to the operating room for evacuation.
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