Pediatric Traumatic Brain Injury: Epidemiology, Pathophysiology, Diagnosis, and Treatment
Pediatric Traumatic Brain Injury: Epidemiology, Pathophysiology, Diagnosis, and Treatment
Authors:
Laleh Gharahbaghian, MD, Clinical Instructor of Surgery / Emergency Medicine; Associate Director, Emergency Ultrasound, Stanford University School of Medicine, Stanford, CA
Bill Schroeder, DO, FAAP, Clinical Instructor of Surgery / Emergency Medicine, Stanford University School of Medicine, Stanford, CA
Robert Mittendorff, MD, Emergency Physician, Kaiser Permanente, Diablo Services Area, Walnut Creek, CA
N. Ewen Wang, MD, Assistant Professor of Surgery / Emergency Medicine; Associate Director, Pediatric Emergency Medicine, Stanford University School of Medicine, Stanford, CA
Peer Reviewer:
Ron Perkin, MD, MA, Professor and Chairman, Department of Pediatrics, The Brody School of Medicine at East Carolina University, Greenville, NC
Pediatric head trauma is a common presenting complaint to the emergency department (ED) and is a major cause of pediatric death and disability. This article will address the epidemiology, pathophysiology, diagnosis, and management of moderate to severe pediatric traumatic brain injury (TBI), with a focus on strategies to improve outcome. Pediatric mild head injuries will be addressed in a future issue of Pediatric Emergency Medicine Reports.
Epidemiology
TBI accounts for a significant number of pediatric deaths, disability, and permanent injury. Pediatric head trauma results in approximately 400,000 ED patient presentations and 30,000 hospitalizations annually.1 Severe pediatric TBI, which ranges between 10% and 30% of annual pediatric head injury presentations, is estimated to have a mortality rate of up to 30%, accounting for approximately 3,000 annual deaths in the U.S. alone. Direct costs related to ED and inpatient hospital care for pediatric TBI exceed $1 billion annually.2
The etiology of TBI varies for different pediatric age groups and developmental stages. Nonaccidental trauma (also termed "abusive head trauma") is a leading cause of severe infant TBI. Falls are the major cause of head injury in preschool-age children. Falls and motor vehicle accidents (MVAs) jointly are the major causes for TBI in children 4–14 years of age. MVAs become the dominant cause of TBI for children 14–18 years of age.3
Pathophysiology
To understand the consequences of brain injury, it is important to understand the physiology of the brain and the requirements for proper brain function. The brain has a high metabolic rate; it consumes 20% of the total oxygen requirement for the body, and 15% of the cardiac output. Proper functioning relies on adequate oxygenation. The amount of oxygen delivered to the brain relies on blood oxygen content, cerebral blood flow (CBF), and cerebral perfusion pressure (CPP), which can be calculated by subtracting intracranial pressure (ICP) from the mean arterial pressure (MAP).
CBF is autoregulated via a pressure-volume relationship in the brain microvasculature. Under normal circumstances, ICP is less than 15 mmHg, MAP is 50-150 mmHg, and CPP is at least 60 mmHg; CBF is generally held constant secondary to physiologic responses to pCO2, pH, and blood pressure. For example, with decreased blood pressure and decreased respiratory rate, the pCO2 increases and pO2 decreases, which results in a decrease of the pH. In an acidotic environment, the cerebral vessels dilate, thus increasing CBF and oxygen delivery to the brain. In the case of severe TBI, autoregulation is disturbed, resulting in a more linear relationship between CBF and MAP and thus increasing ICP. This is assumed to ultimately result in increased CPP when a patient's MAP is poorly controlled.
Brain injury is classified into either direct injury, involving blunt or penetrating trauma to the head resulting in skull fracture, brain contusion, and epidural hematomas; or indirect injury, involving accelerating/decelerating shearing forces, which may have no external signs of trauma but result in a subdural hematoma or diffuse axonal injury. TBI is also categorized in relation to the type and time of brain insult. Primary injury is a direct result of the initial insult or traumatic event, is usually irreversible, and involves the classifications of TBI described above. Secondary injury occurs minutes to days after the initial insult, is preventable, and occurs as a consequence of the primary injury. It results from derangement of normal physiologic processes, both intracranial and systemic. Intracranial derangements include apoptotic or necrotic mechanisms and cerebral edema. Systemic derangements include poorly compensating inflammatory and repair mechanisms, and hypoxia or perfusion abnormalities. (See Table 1.)
Table 1. Summary of Systemic Causes of Secondary Brain Injury and their Physiologic Effects
Systemic Causes of Secondary Injury Physiologic Effect
Hypoxemia* Decreased oxygen delivery
Hypotension* Decreased oxygen delivery
Time to evacuation Decreased perfusion to of hemorrhage** compressed areas
Anemia Decreased oxygen-carrying capacity
Hyperglycemia Increased anaerobic metabolism
Hyperthermia Increased oxygen demand
Seizure Decreased oxygen delivery
Coagulopathy Increased hemorrhage risk
* Associated with doubling morbidity and mortality
** Time to evacuation of intracranial mass: doubles morbidity and mortality if done > 4 hours after initial insult
Increasingly, research has demonstrated that age plays a complicated role in the pathophysiology and outcomes of pediatric TBI. For example, infants have open sutures and a more distensible skull, and therefore can tolerate increasing cerebral edema. Hypotension can occur with large linear skull fractures that result in large epidural hematomas in those younger than 1 year of age. Diffuse cerebral swelling causing increased ICP seems to be more common in children than adults after TBI.4,5
Neuronal development of the pediatric brain continues into the second decade of life. CBF, metabolism, and developmental biomarkers change with age.6,7 There is decreased autoregulation in children younger than 2 years of age. In injury, pediatric brain cells demonstrate a tendency towards apoptosis, and neuroactive medications may have unintended effects. These complex findings translate clinically into increased cerebral swelling in young children, increased incidence of posttraumatic seizures, as well as unpredictable developmental outcomes.
Anatomy
Pathology. Skull Fractures. Childhood skull fractures are common. The incidence of pediatric skull fractures ranges from 2% to 30% of pediatric head trauma ED presentations.8,9 Younger children are at increased risk of injury from skull fracture due to increased quantity of membranous bone, which is thin and more easily fractured, as well as bowing of thin bone, which can result in diastatic fractures or indentation fractures.8
Skull fractures are characterized depending on location, pattern, and complexity. The location of skull fractures are described as either basilar, occurring at the petrous temporal bone, or within the outer skull convexity itself. The pattern is described as either linear, depressed, or comminuted / stellate. Linear fractures can result from falls from low heights and are the most common. They most frequently occur at the parietal bone and rarely cross suture lines. The complexity of skull fractures are described as open, if an associated scalp laceration is present; and depressed, if the skull is depressed by half the height of the skull plate, carrying an increased risk for seizures and meningitis. Skull fractures usually result from impact and force associated with blunt trauma.
Diagnosis of a skull fracture can be made with computed tomography (CT) or skull x-rays. Nondisplaced, linear fractures can be missed on CT scan, as they can be confused with suture lines. Practically, the image finding is less likely to be a fracture if it is bilateral and / or jagged, since fractures most frequently tend to be unilateral and linear. Though scalp hematomas, especially in the subgaleal space, often occur with skull fractures, they have been found in multiple studies to be sensitive (> 90%) but not specific (< 60%) in predicting skull fractures.10
Isolated skull fractures heal without morbidity over a course of months in infants, but can produce a bony prominence similar to a vascular groove.9,11,12 In older children, skull fractures heal over one to three years. Rarely, leptomeningeal cysts can occur when the dura is caught and torn by sharp skull fragments. These cysts require neurosurgical intervention at a later date and serve as a driver to identify all skull fractures in pediatric head trauma patients to ensure appropriate and timely neurosurgical follow-up.
Epidural Hematoma. Epidural hematomas (EDHs) are defined as blood between the dura and the inner skull table. (See Figure 1.) In contrast to adults, EDHs in children are not usually associated with a skull fracture in the temporoparietal area resulting in rupture of the middle meningeal artery. The pediatric skull is more elastic and, therefore, EDHs in children develop near the tentorium as a result of dural sinus tears and can be associated with depressed skull fractures.7
Figure 1. Epidural Hematoma
Diagnosis of an EDH is usually made by CT scan. EDHs follow and are framed by suture lines and appear lens-shaped (biconvex) on CT scan. While CT imaging detects epidural bleeds emergently, magnetic resonance imaging (MRI) can more easily demonstrate EDHs that border the transverse or sagittal sinuses and can more precisely delineate the relation of the bleed to the venous sinuses.8,9 Since EDHs can expand quickly and can result in herniation and subsequent death if not treated aggressively, it is imperative to rapidly diagnose, stabilize, and refer the patient with an EDH to an appropriate trauma center for possible surgical intervention. If diagnosed and treated aggressively, patients with EDHs have a favorable prognosis. An ipsilateral pupillary dilatation with contralateral paralysis is a result of transtentorial or uncal herniation and is a perilous finding.
Figure 2. Subdural Hematoma
Subdural Hematoma. Subdural hematomas (SDHs) are blood collections between the dura and arachnoid layers that often occur as a result of deceleration and shear force injury. (See Figure 2.) They are due to tears in the cortical bridging veins and extravasation of blood into the subdural space. Young infants are at increased risk of such injuries as a result of a more fixed dura. These bleeds can produce significant changes in neurological and clinical status as a result of increased mass and elevated ICP, but may be slower to present than EDHs. Acute SDHs are identified fewer than three days after trauma; subacute SDHs, between three days and three weeks; and chronic SDHs, more than three weeks after trauma. Chronic SDHs may develop septated structures and thick layers that obscure the boundaries and size. Acute SDHs still carry an overall mortality of up to 20%–30%, with a worse prognosis for individuals with other injuries, mass effect, neurological deficits, and delayed surgical treatment.8, 9
Subdural hygromas can also devel-op in the setting of acute trauma. These are collections of cerebrospinal fluid (CSF) in the subdural space, and can be caused by anything that increases the space between the skull and dura, such as atrophy or trauma, and tears the arachnoid, causing CSF to leak into the subdural space. Radiographically, they are defined as any new low-density collection seen on a radiographic study in the context of trauma.13 While subdural hygromas are far more benign than SDHs, they can be difficult to differentiate on CT scan.
Subarachnoid Hemorrhage. While subarachnoid hemorrhage (SAH) can occur secondary to rupture of an arteriovascular malformation (AVM), they also are common in deceleration injuries. SAH results in blood collection beneath the arachnoid and can spread along the arachnoid to adjacent sulci and gyri. (See Figure 3.) SAH can have potent neurologic effects as a result of vasospasm, irritation, and mass effect of the underlying parenchyma.8,9
Figure 3. Subarachnoid Hemorrhage
Cerebral Contusion. Approximately 50% of brain injuries involve a contusion, which results from direct contact between the skull and brain, often with ill-defined margins on imaging. (See Figure 4.) Contusions result more commonly from deceleration injuries and occur more frequently at the base of the frontal, temporal, and parietal lobes, where the brain is in contact with the bony calvarium floor. Traumatic force applied to one part of the bone can produce contusions at distant parts of the brain where bone is bent or flexed in response to the initial force.8 Often, contusions are found not only at the site of impact but also in an area opposite and distant from the site of impact, where it is referred to as a contrecoup injury.
Figure 4. Cerebral Contusion
Diffuse Axonal Injury. Diffuse axonal injury (DAI) involves significant and diffuse disruptions in brain white matter involving the tearing or stretching of neuronal axons. Rotational and torsional force can produce significant axonal disruption, which dramatically affects awareness and consciousness; MVA is one of the most common causes of DAI. DAI is best seen on MRI and appears as multiple, deep-seated elliptical areas of increased signal density within the white matter that spares the cortex. Patients with DAI may have a completely normal CT, but half of these injuries can be seen on CT. The most common appearance is that of small petechial hemorrhages, located at the gray-white matter junction, as well as in the corpus callosum and brainstem.
Vascular Injury. Vascular injury, including stenosis, dissecting aneurysm, and occlusion, can result from the same shear stress forces that produce DAI. Although rare, these injuries can present with significant neurologic abnormalities. Dissection is commonly found in the cervical vertebral arteries and the carotid artery where it bifurcates into the internal and external carotid. Since prevalence rates for such injuries are very low and invasive angiography can be risky and difficult to obtain, noninvasive tests such as CT angiography (CTA) are recommended for initial assessment.
Penetrating Trauma. Although uncommon, penetrating trauma in the pediatric population, as in the adult population, has a poor prognosis. Like adults, injury can be multifaceted and can involve direct trauma from the projectile, indirect trauma from the travel of bony fragments, shockwave-based injury from the projectile wave front, and infection following disruption of the protective layers of brain and exposure to the external environment. In gunshot wounds, the cavity created in the brain is 4–8 times greater than the diameter of the bullet, and damage is a result of transferred kinetic energy to areas outside of the bullet's path. Prognosis depends on the location of the cavity as well as the mass and velocity of the bullet.
Penetrating trauma requires neurosurgical consultation and often results in operative intervention. CT followed by CTA is useful in surgical planning and determining the location of the fragments of bone and other projectiles. Adult patients with penetrating trauma have a rate of vascular injury of 25%–60%.8,14,15
Abusive Head Trauma. Abusive head trauma (AHT) often involves severe, repeated injury associated with a delay in diagnosis and treatment. Intracranial injury in the infant should be considered AHT until proven otherwise, since it is estimated that 50%–90% of TBI in this age group is caused by abuse.11,12,16 Research has demonstrated that AHT causes a unique spectrum of pathology. The most common injuries in AHT are diffuse injuries, such as interhemispheric or tentorial SDH, large nonacute SDHs, and cerebral edema versus focal injuries.
Although SDH is the most common finding, SAH is also a frequent finding.12 Deceleration and shear forces can cause retinal, subarachnoid, or subdural hemorrhages even in the absence of visible external trauma. A skull fracture is found in up to 50% of pediatric patients with intracranial injuries. Stellate or depressed skull fractures should raise the suspicion for AHT.12
Often, the severity of diffuse cerebral injury does not correlate with the severity of the hemorrhage or fracture. Direct and indirect mechanisms play a role in injury related to trauma in infants. Hypoxic / ischemic insults more commonly occur in infants with AHT as opposed to other mechanisms of injury. Other theories hypothesize that hypoxic ischemic encephalopathy results from stretching of the spinal cord, brainstem, or vasculature.17
Evaluation of the Patient with TBI
History. One of the most important ways to evaluate a patient who has sustained head trauma is to obtain a complete and accurate history of the event and mechanism. If the patient arrived by ambulance, EMS personnel should provide information regarding mechanism of injury and if any witnesses or bystanders were present, appearance of the scene where the injury occurred, vitals signs, mental status and initial Glasgow Coma Scale (GCS) level, glucose level, and whether any change in mental status has occurred en route to the hospital. Upon arrival, the patient, if able to talk and provide history, should be asked about the event. However, if the patient is too young, non-verbal, or unconscious, the parents, if present, should be asked of the patient's baseline mental status, past medical history, exposure to toxins or medications, alcohol or drug use, and details regarding the event, which includes mechanism, whether there was loss of consciousness and its length, nausea and vomiting, seizure activity, or abnormal behavior after the incident.
Physical Exam
Physical exam, as in all trauma patients, should follow the algorithm of assessing and managing the airway, breathing, circulation, disability, and exposure ("ABCDE"). Upon evaluation of the airway, rapid sequence intubation should be considered in all patients with severe TBI as well as those who are combative or obtunded. A brief neurological exam should be performed prior to medicating for intubation. Supplemental oxygen should be provided in all patients with suspected TBI upon evaluating for adequate breathing. External hemorrhage, especially scalp lacerations, should be controlled when evaluating for adequate circulation. If poor perfusion is present with hypotension, adequate intravenous access should be established with normal saline fluid boluses ordered and a consideration of other injuries being present, since head injury alone rarely causes hypotension.
Disability is assessed by noting the patient's pupillary response to light, mental status, and general motor function in all extremities. Mental status can be assessed with the AVPU scale (Alert, Verbal, Pain, Unresponsive). The standard for assessing mental status, however, is the use of the GCS as well as its pediatric modification. The patient should be scaled according to their best response. (See Table 2.) TBI is classified based on the GCS level. GCS is 14–15 in mild TBI, 9–13 in moderate TBI, and GCS of ≤ 8 defines severe TBI.
Table 2. Glasgow Coma Scale and Modified Pediatric GCS
Glasgow Coma Scale (GCS)
Eye opening (best response)
Spontaneous 4
To speech 3
To pain 2
None 1
Verbal (best response)
Oriented 5
Confused 4
Inappropriate words 3
Incomprehensible sounds 2
None 1
Motor (best response)
Obeys commands 6
Localizes to pain 5
Withdraws to pain 4
Flexion to pain/ decorticate posturing 3
Extension to pain/ decerebrate posturing 2
None 1
Modified Pediatric GCS
Eye opening (best response)
Spontaneous 4
To speech 3
To pain 2
None 1
Verbal (best response)
Coos, babbles 5
Irritable 4
Cries to pain 3
Moans to pain 2
None 1
Motor (best response)
Normal spontaneous movements 6
Withdraws to touch 5
Withdraws to pain 4
Abnormal flexion 3
Abnormal extension 2
Flaccid 1
Exposing the patient by taking off all clothes and evaluating for external signs of trauma should be done after the ABCD components of the trauma evaluation have been performed. After the primary trauma survey, an exam should be performed from head to toe, with special attention to external signs of injury: scalp lacerations and step offs or crepitus, bulging fontanelle in the infant, and any signs of other systemic injury.
Certain signs of TBI can be present depending on the injury and severity of TBI. Basilar skull fractures frequently present with pathognomic signs, which include Battle sign (periauricular ecchymosis), raccoon eyes (periorbital ecchymosis), nasal CSF leakage, or hemotympanum. Cushing's triad (hypertension, bradycardia and irregular respirations) is a late sign of increased ICP. As the brain herniates, different parts of the brain are compressed; pupillary findings, gross motor abnormalities, and respiration patterns correspond generally with the level of herniation involved. (See Table 3.)
Table 3. Clinical Presentation of Herniation
Herniation
Uncal
Diencephalic
Midbrain
Medullary
Eye Findings
Third cranial nerve com-pression: ipsilateral fixed pupillary dilatation
Small midpoint pupils reactive to light
Midpoint fixed pupils
Dilated and fixed pupils
Gross Motor
Contralateral hemiparesis
Decorticate posturing
Decerebrate posturing
No response to pain
Respiration
Irregular
Apnea alternating with tachypnea (Cheyne-Stokes breathing)
Hyper-ventilation
Apnea
Diagnostic Imaging
Skull Radiographs. Skull radiographs have limited utility in pediatric patients with moderate to severe head injury.
Computed Tomography. CT has revolutionized the evaluation of head trauma. CT readily demonstrates acute hematomas, parenchymal hemorrhage, cerebral edema, skull or facial fractures, hydrocephalus, and herniation. Multi-detector CT can produce high-resolution axial and reformatted images. Rapid scanning also reduces the need for sedation in the pediatric patient or altered patient. Limitations of CT include low contrast resolution, especially of soft tissue. CT also often fails to demonstrate early ischemic changes, axonal injury, and has been found to correlate poorly with long-term clinical outcome for patients with head injuries that are non-hemorrhagic.18,19
Magnetic Resonance Imaging. MRI is a complementary imaging technology to CT. MRI has limited use in the acute trauma setting due to the long duration of the examination and the frequent inability to screen for contraindications to MRI, although this is noticeably more infrequent in the pediatric population. However, MRI often has a role in TBI care after stabilization. MRI shares comparable accuracy with CT in diagnosing subdural or epidural hematomas, but is significantly better at detecting injury of a non-hemorrhagic nature including diffuse axonal injury, cortical contusions, and brainstem injuries. Additionally, MRI more sensitively and specifically provides information on the evolution of injury when compared to CT.
Cranial Ultrasound. Cranial ultrasound (US), an experimental imaging modality when used in the context of neonatal trauma, can demonstrate extra-axial blood collections in many circumstances. As an imaging modality, it has not yet been validated in the acute ED setting.
Physiologic and Functional Imaging. Additional imaging modalities have been developed to evaluate brain physiology. CT perfusion, MR perfusion, or transcranial Doppler imaging can be used to assess perfusion. Multi-detector CT affords the opportunity to image multiple sections of tissue over time with a single contrast bolus. MR spectroscopy can demonstrate lactic acidosis which may play a role in the production of delayed forms of brain injury.
Considerations in the Diagnosis of Brain Injury
Deciding when to image a child with a head injury is an important part of pediatric emergency medicine. This decision is not an easy one, especially in an age of increasing concern with radiation exposure. With serious mechanism and injuries, it is obvious that the risk of injury outweighs the risk of radiation. Any child with significantly altered mental status (most authors agree with an age-adjusted GCS of 13 or less), focal neurologic deficit, or obvious depressed or basilar skull fracture should receive emergent CT imaging. However, in more minor injuries (which are not reviewed in this issue), it is a more difficult decision.
Management of TBI
Pediatric Considerations. The prognosis for pediatric head injuries differs from adult patients due to the child's skull flexibility and pliability, reduced subarachnoid space, different metabolic responses to injury, differences in fluid and edema removal rates, and long term effects from axonal injury. Pediatric skulls are more flexible and so provide less protection to underlying brain, resulting in more brain injury for the same amount of force applied, as compared to an adult skull. The reduced pediatric subarachnoid space allows the brain to move more freely within the skull. Additionally, young children have a larger head-to-body ratio and less neck control/ musculature than do adults. Therefore, it is more likely for a child to suffer a more severe head injury than an adult given the same mechanism and forces. Children generally have a better prognosis than adults do after the same injury, although prognosis is probably age- and injury-dependent. Notably, inflicted brain injuries have worse outcomes and are the most common cause of head injury deaths.20,21
It is important to realize that treatment algorithms of children with severe TBI derive from multidisciplinary guidelines developed in 2003.22 While the guidelines were created upon an evidence-based framework, the authors acknowledged that there are many aspects of pediatric treatment for which there is no high-quality evidence, and thus many recommendations are based on consensus. More recent literature has been published discussing the role of each intervention outlined in the 2003 guidelines, and is described below. Although the primary concern of the emergency physician is the prevention of secondary brain injury, immediate management of primary brain injury should also be considered. Emergent treatment of pediatric TBI consists of two parts: stabilization, diagnosis, and treatment of primary injury; and prevention of secondary injury.
Stabilization, Diagnosis, and Treatment of Primary Injury. Primary injury occurs immediately after head trauma and includes lacerations, hemorrhages, contusions, tissue avulsion, cellular disruption,, and microvascular injury. As always, the ABCDEs of trauma evaluation and stabilization should be performed first, with appropriate spinal immobilization maintenance. Often in the ED, a pediatric patient with a severe TBI will require intubation and advanced monitoring prior to ICU admission. If intubation is required for airway protection, ICP-elevating agents such as ketamine should be avoided. While use of pharmaceuticals (such as lidocaine and fentanyl) to decrease the effects of laryngeal manipulation on ICP have been traditionally recommended prior to administering RSI medications, there is no evidence which supports this practice in children.22 Although there is a theoretical risk of hyperkalemia with nondepolarizing agents like succinylcholine, this is rarely a problem in the trauma patient without pre-existing conditions. Appropriate ventilation must be achieved with care to maximally oxygenate the patient while avoiding hyperventilation. With adequate IV access in place, fluid resuscitation and blood products should be ordered if necessary. After the brief neurologic assessment, interventions to prevent an increase in ICP should be done, as discussed below. Other life-threatening injuries must be identified and ameliorated.
Definitive diagnosis of primary injury will be made by CT imaging. While mass occupying lesions will be treated by surgery, management of non-operable lesions as well as subsequent management of the neurosurgical patient is centered on reduction of elevated ICP, as pathologically elevated ICP is known to cause increased morbidity and mortality in children with TBI.
Prevention of Secondary injury. Secondary injury occurs minutes to days after head trauma, is preventable, and usually is a result of poor oxygenation of the brain. (See Table 1.) Prevention of hypoxia by providing supplemental oxygen or intubation can maximize oxygen delivery to the brain. Appropriate IV access and volume resuscitation are essential to avoid secondary brain injury resulting from poor perfusion caused by hypotension. Blood oxygen carrying capacity should be maximized by maintaining the hematocrit and hemoglobin > 30% and > 10 gm/dL, respectively.23 In children, significant blood loss can result in a precipitous and late-occurring hypotension, since children can often maintain blood pressures with extreme volume loss until compensatory mechanisms are exhausted. In this situation, the practitioner should focus on preparing resuscitative solutions, giving blood products via rewarmer circuits, and use massive transfusion guidelines if needed to maintain adequate volume and optimal cerebral perfusion pressures. Monitoring of the urine output (target is > 1 mL/kg/hr), heart rate, and peripheral pulses can be used in addition to blood pressure to ensure adequate volume resuscitation.22 To decrease oxygen demand, hyperthermia should be corrected and hyperglycemia should be corrected using regular insulin subcutaneously, with a goal glucose level of < 200 mg/dL. Seizures should be treated with benzodiazepines and prevented in severe TBI using phenytoin or fosphenytoin. Coagulopathy should be corrected as to avoid increasing intracranial hemorrhage. Morbidity and mortality doubles with persistent hypoxia and hypotension and should be avoided.24 Figure 5 outlines a consensus algorithm for management of elevated ICP.
Figure 5. Consensus Algorithm for Management of Elevated ICP in Pediatric TBI
Key: GCS, Glasgow Coma Scale; ICP, intracranial pressure; CPP, cerebral perfusion pressure; HOB, head of bed; CSF, cerebrospinal fluid; CT, computed tomography; PRN, as needed.
Used with permission from: Adelson PD, et al. Critical pathway for the treatment of established intracranial hypertension in pediatric traumatic brain injury. Pediatr Crit Care Med 2003;4 (3 Suppl):S66.
Operative Management. A neurosurgeon should be consulted for any intracranial bleeding or depressed skull fractures. Expedient transport to an appropriate trauma or neurosurgical critical care center is vital if these resources are not locally available. Although not commonly considered within the scope of the emergency physician's practice, burr holes and intraventricular drains are potential options, in consultation with the neurosurgeon, to lower ICP when transport distance to a neurosurgical center is far and where mass effect is causing dramatic neurologic decline, GCS < 8, and increasing mass effect.
CPP Management. Specific TBI management is focused on maintaining adequate blood oxygen delivery to the brain.40 MAP should be optimized with volume resuscitation in order to maintain CPP. (See Table 4.) It is important to note that improved CPP depends on intact autoregulation mechanisms in the cerebral vasculature and if autoregulation is disrupted, a linear relationship occurs between CBF and MAP. The CPP should be > 40 mmHg and ICP should be < 20 mmHg.
Table 4. Cerebral Perfusion Pressure Equations
- CPP = MAP – ICP (goal: 60)
- MAP = 1/3 SBP + 2/3 DBP (goal: 60)
- ICP = 1-15 mmHg
Key: CPP, cerebral perfusion pressure; MAP, mean arterial pressure; ICP, intracranial pressure; SBP, systolic blood pressure; DBP, diastolic blood pressure
Retrospective data demonstrate that patients with a CPP < 40 mmHg have worse outcomes than patients with a CPP > 40 mmHg24, and the 2003 guidelines recommend the maintenance of a continuum of CPP of 40–65 mmHg in infants and adolescents accordingly.22 There are no robust prospective data to date that offer optimal age-related CPP cut-offs.
Interventions to Decrease Elevated ICP
Increased ICP can be difficult to diagnose in young children and infants. Significant variations in the treatment of severe TBI continue to exist, especially in regards to ICP-guided therapy. This variability in treatment results mainly from a paucity of data from which to create standards and from the heterogeneity inherent in pediatric TBI. The approach to management of severe TBI based on the published guidelines should be focused on ICP control, and ultimately improve CPP.21 Interventions to prevent an increase in ICP should be performed on all patients suspect of TBI. Interventions to actively decrease ICP are most commonly done in the acutely decompensating patient with suspected herniation and should be performed with extreme caution when there is no ICP monitoring available. Signs and symptoms of elevated ICP include unilateral fixed and dilated pupil, change in mental status, motor posturing, papilledema, bulging fontanelle, Cushing's reflex, and hemodynamic instability that has no other etiology. ICP monitoring is indicated in consultation with a neurosurgeon for GCS < 8 and has been shown to correlate with improved outcome.22 Pathologically increased ICP in children is defined as an ICP ≥ 20 mmHg. While ICP threshold may be lower for young children, there is no current data to support this statement.22
Head Position. The patient's head should be kept in a neutral position, especially if concerns about spinal cord injury exist. Increasing the head of the bed (HOB) to 30° is recommended to decrease ICP while maintaining MAP. Care should be taken to not tape endotracheal or other tubes in a manner that may cause jugular venous congestion, since this can increase ICP. Additionally, correct positioning of the head of an infant often requires elevation of the shoulders. A shoulder roll to maintain an anatomic head, neck, and torso position is encouraged.
Neuromuscular Paralysis, Sedation and Pain Medication Management. Appropriate sedation, pain management, and paralysis will afford the opportunity to stabilize the patient for ventilation, scanning, and other invasive procedures. A brief but thorough neurologic examination should be recorded, if possible, prior to neuromuscular blockade since this can have an effect on subspecialist management decisions. Sedative agents must always be used during the period of paralysis, and pain management should be achieved with short-acting opiates concurrently.23 Short-acting agents like midazolam and fentanyl allow the emergency physicians or consultants to perform periodic neurologic examinations.
Hyperosmolar Agents. Osmotic agents such as mannitol or hypertonic (3%) saline can be used in the setting of impending herniation or dramatic clinical or neurological decline.22,23 Mannitol and hypertonic saline decrease the viscosity of blood and reduce extravascular volume, which is directly correlated with ICP.22 Mannitol is an osmotic agent that has traditionally been given as boluses of 0.25–1 g/kg body weight every 2–8 hours (the onset is within 30 minutes and half life is 3–4 hours). However, without adequate volume resuscitation, diuresis can cause hypovolemia and hypotension. Mannitol may also cross the disrupted blood-brain barrier and cause increased ICP.25 Hypertonic saline 3% given as a bolus (0.10–1 mL/kg body weight) or as an infusion (0.10–1 mL/kg body weight per hour) has gained popularity as an agent to decrease ICP.22,26 Hypertonic saline does not cause diuresis, although if infused too rapidly, it could cause increased ICP. The theoretical advantage of hypertonic saline is that it can be administered to hemodynamically unstable patients with impending herniation because it preserves intravascular volume. Hypertonic saline can also increase osmolality. Its complications include osmotic demyelinization syndromes, acute renal insufficiency in the setting of elevated osmolality above goal, and coagulopathy.21
Hyperventilation and Hypocapnea. Normocarbia is important to cerebral perfusion, maintaining normal ICP, and optimizing the oxygen-carrying capacity of hemoglobin. Intubation may help maintain normocarbia.
Hyperventilation and hypocapnea acts in seconds, peaks at 6–8 minutes, and should only be used in the setting of impending herniation such as dramatic clinical or neurologic decline (extensor decerebrate) posturing, flaccid response (1 on GCS motor score), asymmetric pupils, dilated and non-reactive pupils, or a decrease in GCS of more than two from prior best score (in patients with an initial GCS less than 9), since it is only temporizing and can lose its effect over time.23 When signs of elevated ICP are present, reducing the pCO2 to 30–35 mmHg resulting in hypocarbia causes vasoconstriction and, thus, a decrease in CBF. Although lowering the pCO2 too much can result in parenchymal ischemia, it can also reduce ICP by as much as 25%.22,27
Seizure Prophylaxis. Anti-epileptic medications should be used in patients suffering from severe TBI with significant injury to the brain on CT. (See Table 5.) Patients with traumatic seizures should be loaded with phenytoin in the ED.28
Table 5. Indications for Seizure Prophylaxis in Patients with Severe Head Injury
- Depressed skull fracture
- Paralyzed and intubated patient
- Seizure at the time of injury
- Seizure in the ED
- Penetrating brain injury
- Severe head injury (GCS < 8)
- Acute subdural hematoma
- Acute epidural hematoma
- Acute intracranial hemorrhage
- Prior history of seizure
Glucose Control in TBI. Hyperglycemia is a common stress response. However, hyperglycmia can cause increased infection, inflammation, and higher in-hospital mortality.29
Alterations in glucose homeostasis in the pediatric ICU have shown that hyperglycemia and glucose variability are associated with increased mortality and morbidity. While tight glycemic control has been associated with improved outcomes, it has also been associated with an increased risk of hypoglycemia in adult ICU patients.29-31 Thus, care should be taken to ensure that pediatric TBI patients are maintained euglycemic in the ED.
Steroids in Head Trauma. Steroids have no role in the acute management of pediatric TBI. There are no prospective, randomized studies that demonstrate improvements in outcome with the use of steroids, and there is critical care evidence that demonstrates increased infection rates with the provision of steroids.22,23
Hypothermia. Hypothermic treatment is not supported by current evidence. While earlier studies demonstrated that hypothermia may play a role in injury mitigation,32-35 a large, prospective, multi-center trial demonstrated no improved neurological outcome and increased mortality in TBI children receiving hypothermic treatment.36
While the role of hypothermia is still controversial, it is important to prevent hyperthermia and to focus on the maintenance of normothermic conditions. The mechanism of hyperthermia as it relates to secondary injury is multifaceted and involves increasing metabolic rates, cellular energy, and oxygen requirements; increased production of inflammatory mediators; increased neuronal excitation; and increased rate of necrotic or apoptotic cell death. Higher temperatures also lower the seizure threshold, which, if seizures occur, can also cause the aforementioned effects.
Antibiotics. Antibiotics play no role in closed head injuries. Open-skull fractures and penetrating head injuries are at higher risk for infection and can be treated with a short course of a first-generation cephalosporin for coverage of Staphylococcus epidermidis or S. aureus. An IV dose of antibiotics should be given to cover these pathogens prior to the placement of an ICP monitoring device in the ED.
CSF Drainage. The theory that drainage of CSF by repeated lumbar puncture or by the placement of lumbar drains to decrease ICP is highly controversial. Currently, it is only described when first- and second-line interventions have failed.21
Disposition
For a child with altered mental status, seizure, or radiographic evidence of intracranial injury, admission is required and observation in the ICU is highly recommended. If sufficient facilities or personnel are unavailable, the pediatrics or ICU service in conjunction with the ED physician should transfer the patient to an appropriate hospital or trauma center.22,37-40 Repeat head CTs are not useful unless there is a surgical indication or clinically significant reduction in mental status.18,41-46
Conclusion
Pediatric TBI is a significant cause of childhood mortality and morbidity. Treatment parameters are based on guidelines written in 2003 by a multi-disciplinary group of experts. There is little Class I evidence to support these guidelines; rather, many were developed by consensus and extrapolation of adult studies with the realization that pediatric TBI has different pathophysiologies with different etiologies in children of different ages. In summary, emergency management of pediatric TBI should focus on preventing secondary brain injury resulting from hypoxia, hypotension, hyperglycemia, hyperthermia, seizure, coagulopathy, and increased ICP. Finally, children with TBI have improved survival, and thus should be cared for in pediatric trauma centers or adult trauma centers with pediatric expertise.22,25,47
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Pediatric head trauma is a common presenting complaint to the emergency department (ED) and is a major cause of pediatric death and disability. This article will address the epidemiology, pathophysiology, diagnosis, and management of moderate to severe pediatric traumatic brain injury (TBI), with a focus on strategies to improve outcome.Subscribe Now for Access
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