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Part 2 book Pediatric critical care medicine (Volume 4: Peri-operative care of the critically ill or injured child) includes: Trauma, cardiac surgery and critical care, critical care of the solid organ transplant patient.
Part III Trauma Richard A Falcone Head and Neck Trauma 14 Derek S Wheeler, Derek Andrew Bruce, and Charles Schleien Abstract While the overall mortality rates have decreased significantly, TBI remains a significant public health problem In addition, while cervical spine and spinal cord injuries are less common in children compared to adults, these injuries are an important source of long-term morbidity and pose a significant burden on the health care system The management of these injuries has continued to evolve over time Critically injured children with TBI require the close coordination of management between the PICU team, the trauma surgeon, and the neurosurgeon Keywords Traumatic brain injury • Depressed skull fracture • Closed head injury • Cervical spine injury • SCIWORA • Spinal cord injury • Epidural hematoma • Subdural hematoma • Intracranial hypertension Introduction Trauma is the leading cause of pediatric morbidity and mortality in the United States The mortality rate due to trauma has declined significantly in all age groups since 1979, largely as a result of aggressive injury prevention programs However, accidental injury still accounts for more than one-third of all childhood deaths [1] Many of these D.S Wheeler, MD, MMM (*) Division of Critical Care Medicine, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, 3333 Burnet Avenue, Cincinnati, OH 45229-3039, USA e-mail: derek.wheeler@cchmc.org D.A Bruce, MB, ChB Center for Neuroscience and Behavioral Medicine, Children’s National Medical Center, 111, Michigan Avenue NW, Washington, DC 20010, USA e-mail: dbruce@childrensnational.org C Schleien, MD, MBA Department of Pediatrics, Cohen Children’s Medical Center, Hofstra North Shore-LIJ School of Medicine, 269-01 76 Ave, Suite 111, New Hyde Park, NY 11040, USA e-mail: cschleien@nshs.edu D.S Wheeler et al (eds.), Pediatric Critical Care Medicine, DOI 10.1007/978-1-4471-6359-6_14, © Springer-Verlag London 2014 deaths are due to traumatic brain injury (TBI) [2] Neck and cervical spinal cord injuries, although relatively rare in the pediatric population, often have catastrophic consequences [3–5] Clearly, pediatric head and spinal cord trauma creates a significant burden on society Head Trauma Epidemiology While the overall mortality rates have decreased significantly, TBI remains a significant public health problem Seat-belt and bicycle helmet laws have resulted in a dramatic decrease in both the number and severity of TBI in children [6, 7] Although children generally have better survival rates than adults [6], the life-long sequelae of even a mild TBI can be more devastating in children due to their young age and developmental potential [8, 9] The usual mechanism of injury depends on the age of the patient For example, children under years most often suffer TBI secondary to falls, motor vehicle accidents, or non-accidental trauma (child abuse), while TBI in older children usually occurs second199 200 ary to sporting or motor vehicle accidents In the adolescent population, motor vehicle accidents and assault or violent crime are the most common causes of TBI [6, 9] Males appear to sustain TBI almost twice as often as females, especially in the adolescent age group Most large series show an increased incidence of head trauma in the spring and summer months when children are more likely to be outdoors [10] As mentioned above, pediatric TBI is a significant burden to the health care system, accounting for more than $1 billion in total hospital charges every year in the United States alone These costs not take into account the costs of future medical care, years of lost work, and the years of lost quality of life, which are likely to be significantly greater [11] Physical abuse (inflicted trauma) is the leading cause of serious head injury and death in children under years of age [12] The mechanism of injury in inflicted or abusive head trauma is controversial, but likely involves a combination of shaking, asphyxia, and blunt trauma to the head The distinction between inflicted and accidental head injury in young children is important as it greatly affects prognosis Outcome among children with non-accidental head trauma is significantly worse, and the majority of survivors suffer significant disability and neurologic impairment [13] Inflicted or abusive head trauma is discussed in greater detail elsewhere in this textbook Pathophysiology The pathophysiology of TBI is specific to either the primary or secondary insult Primary injury is the injury that results directly from the original impact and is best prevented by aggressive injury prevention programs, including the proper use of safety devices such as seatbelts, bicycle helmets, and air bags Primary head injury can involve damage to the scalp, cranial bone, dura, blood vessels, and brain tissue as a result of immediate application of acceleration/deceleration forces with or without impact Both contact and inertial forces may be involved in the primary injury Linear force vectors occur when the head is struck by a moving object and are responsible for generating contact force Inertial forces are created by acceleration/deceleration or angular-rotational movement of the head in space Because the child’s headto-torso ratio is much greater than that of the adult, inertial forces are magnified in children resulting in more diffuse brain injury The relatively higher water content and incomplete myelination of the pediatric brain may also contribute to the diffuse nature of the injury in the immature brain as compared to the more focal adult pattern [14] Impact injuries to a static head have their greatest effects on the skin and skull and, as a result of absorption of the force by these tissues, less effect on the brain tissue and brain blood vessels For example, children with depressed skull fractures may have an associated cerebral contusion, though D.S Wheeler et al the predominant damage occurs to the skull Acceleration/ deceleration forces, whether associated with impact or not, result in complex deformations of the brain and its blood vessels that can lead to a variety of pathologies from (i) shearing injury of the white matter, with or without hemorrhage, (ii) contusion or laceration of the cortex or deep structures, including the midbrain and medulla, (iii) disruption of arteries or veins with subsequent hemorrhage, and (iv) disruption of the blood-brain barrier Secondary brain injury results from the physiologic and biochemical events that occur after the initial trauma or primary brain injury The best recognized of these secondary injuries are systemic hypotension, hypoxemia, hypercarbia, intracranial hypertension, and cerebrovascular spasm Hypotension and hypoxia commonly present on admission to the emergency department (ED) and thus any secondary damage may already have been sustained prior to advanced medical care (i.e., in the ED or PICU) However, intracranial hypertension tends to progress over several days and is rarely present during the early stages after initial resuscitation Other secondary injuries may be produced by a variety of molecular events (discussed elsewhere in this textbook in much greater detail) such as the release of excitotoxic neurotransmitters or free oxygen radicals Multiple mechanisms have been implicated in secondary brain injury and include cerebral ischemia, release of excitatory neurotransmitters, free radical formation, activation of neuronal apoptosis cascades, and blood-brain barrier disruption leading to cerebral edema The role of these mechanisms in human brain trauma is unclear and no specific therapies are available to correct or modify these molecular events In children, cerebral blood flow (CBF) is reduced shortly after TBI Loss of endogenous vasodilators such as nitric oxide and elaboration of vasoconstrictors such as endothelin1 have been implicated in producing post-traumatic hypoperfusion Glutamate levels in cerebrospinal fluid have been shown to increase in humans after brain injury leading to excitotoxic neuronal death in cell culture Glutamate exposure leads to elevation of intracellular calcium, oxidative stress, and production of free radicals Although a portion of cell death occurs immediately after the initial insult, some neurons have been shown to die in a delayed manner by apoptosis [15] The immature brain may be more vulnerable to apoptosis as demonstrated in experimental animal models where the severity of neurodegeneration after trauma was highest in the youngest animals [16] Finally, both osmolar swelling in contusions and astrocyte swelling as a result of excitotoxicity contribute to significant cerebral swelling This swelling can lead to secondary ischemia and/or herniation with their devastating consequences Post-traumatic insults such as hypoxia and systemic hypotension are common in children and are known to exacerbate the severity of secondary injury and worsen 14 Head and Neck Trauma prognosis [17–19] Since intracranial hypertension, hypoxia, and systemic hypotension are the leading factors associated with poor outcome, post-injury interventions which decrease or ameliorate these events reduce secondary injury to the injured but still viable brain Trauma Systems The influence of trauma systems and pediatric trauma centers on outcomes of TBI has recently been studied Children with severe TBI are more likely to survive if treated in a pediatric trauma center or an adult trauma center with added qualifications to treat children [20–24] Based on the wealth of experience, pediatric patients in a metropolitan area with severe TBI should be transported directly to a pediatric trauma center which will most likely be in close proximity to the accident site [25, 26] However, for those children injured in rural areas, stabilization at an outside hospital may be indicated prior to transfer to the trauma center Initial Resuscitation Immediate attention to airway, breathing, and circulation is mandatory for all unconscious children The initial resuscitation of a child with TBI is vitally important since post-injury hypoxia and systemic hypotension are associated with worse outcome (as discussed above) It may be possible to minimize the rate of occurrence of these events with proper early resuscitation measures Generally all resuscitation interventions are aimed at lowering intracranial pressure (ICP) and maximizing cerebral perfusion pressure and delivery of oxygen and substrate to the brain Providing the injured brain with adequate substrate to maintain normal function is dependent on maintaining a stable airway, adequate ventilation, cardiac function, and systemic perfusion (i.e., airway, breathing, circulation) Hypotension, defined as systolic blood pressure less than 5th percentile for age, has been associated with a 61 % mortality rate in children with severe TBI and an 85 % mortality rate when combined with hypoxia [27] Hypotension has repeatedly been shown to worsen the prognosis for all levels of severity (as determined by the Glasgow Coma Score, GCS) of central nervous system (CNS) injury in children as well as in adults [17–19, 27–32] Hypotension is present at admission in 20–30 % of severe head injuries and the avoidance of hypotension, if possible is dependent on timely recognition and resuscitation prior to arrival to the hospital Episodes of hypotension can also occur in the hospital, both in the ED and in the PICU The origin of these episodes is unclear and therefore avoiding them may be difficult However, close, intensive multimodality monitoring will identify these 201 episodes early and allow for timely intervention While hypotension must always trigger a careful exploration for possible areas of blood loss, it can occur with isolated head injury or spinal cord injury [33] Regardless of the etiology, hypotension must be aggressively treated TBI can be associated with loss of normal cerebral autoregulation (Fig 14.1), such that rapid decreases in mean arterial pressure (MAP) result in profound decreases in cerebral perfusion pressure (CPP) and cerebral blood flow (CBF) Since children will often maintain their systolic blood pressure despite significant blood loss until they enter the later stages of hypovolemic shock, clinical signs of shock (such as tachycardia, diminished central pulses, urine output less than mL/kg/h, cool extremities, and prolonged capillary refill) should be treated as if hypotension were already present and rapidly corrected with volume resuscitation Fluid restriction to avoid exacerbating cerebral edema is contraindicated in the management of the child with TBI in shock The use of hypertonic saline as a resuscitation fluid is gaining popularity because of the beneficial effects on ICP, though there are no clinical trials to support this type of fluid over other available agents for fluid resuscitation Transfusion of packed red blood cells is indicated to replace active blood loss, though the ideal transfusion trigger for critically injured children with TBI is not known [34–36] Severe anemia is potentially harmful in patients with TBI Furthermore, transfusion can help maintain intravascular volume and maximize oxygen carrying capacity However, observational and retrospective studies have shown that transfusion does not necessarily improve short- and longterm outcomes [37–39] Regardless, once the volume deficit has been corrected, a vasopressor (e.g., dopamine, epinephrine) should be administered to patients with persistent hypotension Resuscitation fluid should be isotonic to avoid the risk of worsening cerebral edema It is recommended that intravenous glucose be avoided in the first 48 h after injury as hyperglycemia has been associated with worse outcome [40] However blood glucose should be monitored frequently, especially in younger children who are most at risk for hypoglycemia The deleterious effects of hypoxia are less well established (compared to hypotension), though there is evidence to suggest that post-injury hypoxemia, defined as PaO2 1 mm Apnea, bradypnea, irregular respirations Loss of gag/cough reflex Cervical spine injury with respiratory compromise Inadequate oxygenation or ventilation children with a GCS ≤8 should have their airway secured by tracheal intubation to avoid hypoxemia, hypercarbia, and aspiration (Table 14.1) Ideally, this should be performed by an individual with specialized training in the pediatric airway and with the use of capnometry/capnography to verify proper placement of the airway in the trachea (please see the chapters on Airway Management for a more in-depth discussion of this topic) These specifications are made for children because success rates of prehospital tracheal intubation in children have been shown to be lower than in adults The cervical spine must be stabilized in the midline during tracheal intubation in any child with suspected cervical spine injury Children with TBI should be ventilated with the goal of maintaining PaCO2 in the normal range Aggressive hyperventilation to acutely reduce PaCO2 should be reserved for the acute situation when signs of impending brain herniation 14 Head and Neck Trauma CT is still better at defining the extent of bony injury However, until faster MRI scanners become available and more MRI compatible equipment is developed, CT remains the initial imaging study of choice [46] The results of this initial CT dictate the next steps in management If there is a significant mass lesion (e.g., epidural hematoma), surgery is usually required However, if there is no mass lesion, the CT scan is further examined for evidence of diffuse axonal injury, ischemic injury, or signs of brain swelling (either focal or generalized) Imaging studies of other organ systems may dictate the need for surgery as well, e.g intestinal rupture If surgery is necessary on other organ systems in a child with a GCS ≤8, insertion of an ICP monitor at the commencement of the operative procedure is indicated, as ICP monitoring allows the anesthesiologist to monitor ICP and to control it until surgery on these other organ systems is completed ICP Monitoring No randomized controlled trials evaluating the effect on outcome of severe TBI with or without ICP monitoring have been conducted in any age group However, ICP-focused intensive management protocols have almost certainly improved outcomes [26, 47, 48] Given the paucity of pediatric data, the current recommendations for pediatric ICP monitoring are largely based upon anecdotal experience and adult studies Indeed, the current pediatric guidelines [26] not make any firm recommendations and suggest that ICP monitoring may be considered for critically injured children with severe TBI (generally defined as GCS ≤8) This recommendation applies to infants as well since the presence of open fontanels and/or sutures does not negate the risk of developing intracranial hypertension nor does it alter the utility of ICP monitoring Although ICP monitoring is not routinely recommended for infants and children with less severe injury (GCS ≥8), it may be considered in certain conscious patients with traumatic mass lesions or for patients whose neurologic status may be difficult to assess serially because of sedation or neuromuscular blockade, especially when going to the operating room for general anesthesia Once the decision is made to invasively monitor a patient’s ICP, there are several types of monitoring devices that can be used These are discussed elsewhere in this textbook The ventricular catheter has been shown to be an accurate way of monitoring ICP and has the added advantage of enabling cerebrospinal fluid (CSF) drainage, making it the preferred method Intraparenchymal monitoring devices are used commonly but have the potential for measurement drift and not allow for CSF drainage Morbidities related to all of these catheters, including infection, hemorrhage, and seizure are unusual 203 Intracranial Hypertension Intracranial pressure, or the pressure within the intracranial vault, is determined by the interactions between the brain parenchyma, the cerebrospinal fluid (CSF), and the cerebral blood volume The fundamental principles of intracranial hypertension were proposed by the two Scottish physicians Monro and Kellie in 1783 [49] and 1824 [50], respectively, who stated that (i) the brain is enclosed in a non-expandable, relatively rigid space; (ii) the brain parenchyma is essentially non-compressible; (iii) the volume of blood within the skull is nearly constant; and (iv) a continuous outflow of venous blood is required to match the continuous inflow of arterial blood However, as originally proposed, the Monro-Kellie doctrine did not take into account the volume of the CSF As we now know, reciprocal volume changes of the CSF compartment is an important compensatory mechanism that will allow reciprocal changes in the volumes of the other cranial compartments (i.e., blood, brain) [51] The combined volume of all of the components of the skull cavity (brain, blood, CSF) must remain constant because they are encased in a fixed volume Therefore, if the volume of one intracranial element increases, the volume of another (e.g CSF) must decrease to compensate and keep ICP in the normal range ICP is therefore a reflection of the relative compliance of the cranial compartments (Fig 14.2) As shown in Fig 14.3, ICP will remain normal in spite of small additions of extra volume, whether edema, tumor, hematoma, etc However, once a critical point is reached, at which compensatory mechanisms are maximized, addition of subsequent volume produces a dramatic rise in ICP During the initial hours following head injury, there is a diminished volume of intracranial CSF as a result of displacement of CSF into the spinal subarachnoid space, as well as increased reabsorption of brain CSF by the choroid plexus Intracranial pressure therefore remains in a safe, normal range However, as edema worsens or hemorrhage increases in size, these compensatory mechanisms eventually fail and ICP increases If cerebral herniation occurs at the foramen magnum or the tentorium (Fig 14.4), the normal CSF pathways are blocked and displacement of CSF cannot occur, resulting in a further decrease in intracranial compliance and worsening intracranial hypertension The perfusion of the brain, like all organs, is determined by the difference between the upstream and downstream blood pressures (i.e perfusion pressure) The driving force for blood flow to the brain (upstream pressure) is the mean arterial pressure (MAP) and the downstream pressure, under normal physiologic circumstances, is the central venous pressure (CVP) In the case of intracranial hypertension, when the ICP exceeds the CVP, the cerebral perfusion pressure (CPP) becomes: CPP = MAP – ICP Therefore, in order to maximize cerebral blood flow (CBF) after TBI, therapies 204 D.S Wheeler et al Venous blood Mass/edema Mass/edema Arterial blood Arterial blood Arterial blood Brain Brain Brain Normal Compensated Uncompensated p c a CSF Venous blood CSF Intracranial pressure Fig 14.2 The Monro-Kellie Doctrine See text for detailed explanation b V Fig 14.3 Pressure-volume curve of the craniospinal compartment This figure illustrates the principle that in the physiological range, i.e near the origin of the x-axis on the graph (point a), intracranial pressure remains normal in spite of small additions of volume until a point of decompensation (point b), after which each subsequent increment in total volume results in an ever larger increment in intracranial pressure (point c) (Reprinted from Andrews and Citerio [51] With permission from Springer Science + Business Media) must be targeted to optimize MAP and reduce ICP thereby decreasing the risk of secondary brain injury It is well known that intracranial hypertension is associated with poor neurologic outcome and that aggressive treatment of elevated ICP is associated with the best clinical outcomes As stated above, approximately 30–50 % of head injuries will demonstrate normal to minimally elevated ICP in the face of adequate CPP and not require any specific therapy directed to the cranial injury [42–45, 52] Management of these patients is therefore directed towards maintaining cardiorespiratory and hemodynamic stability The current pediatric guidelines state that treatment efforts directed towards intracranial hypertension may be considered when ICP >20 mmHg Similarly, the Brain Trauma Foundation and the European Brain Injury Consortium guidelines also recommend initiating treatment of intracranial hypertension if ICP ≥20 mmHg to maintain CPP in the range of 50–70 mmHg [53–55] Two quite different approaches have been proposed for the treatment of intracranial hypertension to prevent secondary cerebral ischemia One approach (presented above) focuses on maintaining the CPP = MAP – ICP in an acceptable range (i.e CPP is increased by either reducing ICP, increasing MAP, or a combination of both) [56–62], while the other approach focuses on decreasing the end capillary pressure in the brain and thus reducing brain edema by slightly lowering arterial pressure and controlling end-capillary pressure and colloid osmotic pressure (the so-called Lund concept) [63–66] Most intensive care units use a combination of these therapies [67, 68] Both methods have their (at times passionate) proponents However, there is insufficient evidence to support one method over the other at this time [69–72] In a single-center observational study comparing ICP and survival, of the 51 children with severe closed head injury who underwent ICP monitoring, 94 % of the children in 14 Head and Neck Trauma 205 consensus guidelines [26] For additional discussion and a detailed reference list of supportive evidence, the reader is referred to these guidelines and the chapter on Intracranial Hypertension in this textbook M1 A B M2 C Fig 14.4 Schematic representation of herniation syndromes According to the Monro and Kellie doctrine, increased volume and pressure in one compartment of the brain may cause shift of brain tissue to a compartment in which the pressure is lower M1 is an expanding supratentorial lesion; M2 is an expanding mass in the posterior fossa A Increased pressure on one side of the brain may cause tissue to push against and slip under the falx cerebri toward the other side of the brain, B Uncal (lateral transtentorial) herniation Increased ICP from a lateral lesion pushes tissue downward, initially compressing third cranial nerve and, subsequently, ascending reticular activating system, leading to coma, C Infratentorial herniation Downward displacement of cerebellar tissue through the foramen magnum producing medullar compression and coma (Reprinted from Citerio and Andrews [205] With permission from Springer Science + Business Media) whom the ICP never exceeded 20 mmHg survived This is in sharp contrast to the 59 % survival rate in the children with maximum ICP’s greater than 20 mmHg [73] An elevation of ICP for greater than hour was found to be most deleterious and was associated with worse clinical outcome This study, and others of its kind have led to the recommendation that treatment for intracranial hypertension should begin at an ICP of 20 mmHg or greater Maintenance of adequate CPP is important in order to allow for ongoing delivery of metabolic substrates to the brain Again, there are insufficient data to establish firm, consensus recommendations [26], though a minimal CPP of 40–50 mmHg may be considered for children The pediatric consensus guidelines further suggested that the appropriate CPP may be age-based – the lower end of the aforementioned threshold is considered appropriate for infants while the upper end is considered appropriate for adolescents A stepwise approach to the management of ICP and CPP was proposed in the original pediatric consensus guideline [25], which is still useful Here we will present a very brief overview of the current pediatric Sedation, Analgesia and Neuromuscular Blockade The use of sedatives and analgesics in the setting of raised ICP remains a difficult challenge Pain and stress are known to increase cerebral metabolic demands as well as cause intracranial hypertension However, most sedatives cause a reduction of mean arterial pressure which can decrease CPP Additionally, these medications may exacerbate an elevated ICP by causing cerebral vasodilation, which in turn increases cerebral blood volume Long-acting sedatives also may interfere with the ability to follow serial neurologic exams For these reasons, short-acting agents like midazolam are preferred Narcotics such as morphine or fentanyl can be used for pain control Medications known to raise ICP, for example ketamine, should be avoided Neuromuscular blocking agents may be used to reduce ICP by preventing shivering, posturing, and breathing against the ventilator (dysynchrony) Potential harmful effects include masking of seizure activity and increased infection risk Therefore, these agents should be reserved for specific indications and only with continuous EEG monitoring In addition, positioning the patient with the head elevated to 30° in a midline, neutral position will facilitate adequate venous drainage through the jugular veins, helping to reduce ICP CSF Drainage CSF drainage can be used as a means of controlling ICP if a ventriculostomy catheter is in place A lumbar drain may be considered as an option for refractory intracranial hypertension if a functioning ventriculostomy is already present Since the lateral ventricles are often small in brain injured patients and up to 30 % of the compliance of the CSF system is in the spinal axis, lumbar drains have been studied as an alternate way of diverting CSF and lowering ICP In a retrospective analysis of 16 pediatric patients, Levy et al reported a decrease in ICP in 14 of 16 children and improved survival after placement of a lumbar drain [74] Hyperosmolar Therapy Osmotic diuretics, such as mannitol, have been used extensively in the management of intracranial hypertension Mannitol (0.25–1 g/kg IV) is effective in lowering ICP both by decreasing blood viscosity and thereby decreasing cerebral blood volume, and by gradually drawing water from the brain parenchyma into the intravascular space This effect however requires an intact blood-brain barrier which may not be present in injured areas of the brain Mannitol may therefore leak into the injured area and accumulate, exacerbating 206 focal edema Other risks of mannitol use include acute tubular necrosis and renal failure, perhaps related to hypovolemia and dehydration Care should be taken to maintain euvolemia and serum osmolarity below 320 mOsm/L Hypertonic, % saline is effective in controlling ICP with few adverse effects at doses of 0.1–1.0 mL/kg/h The current consensus pediatric guidelines favor hypertonic saline over mannitol at doses between 6.5 and 10 mL/kg for acute increases in ICP [26] A continuous infusion is an acceptable alternative It appears that hypertonic saline can be safely used up to a serum osmolarity of 360 mOsm/L Hyperventilation Prophylactic hyperventilation is contraindicated in the setting of pediatric TBI Hypocapnia induces cerebral vasoconstriction and leads to a reduction in cerebral blood volume and ICP Chronic hyperventilation depletes the brain’s interstitial bicarbonate buffering capacity and causes a shift in the hemoglobin-oxygen dissociation curve, impairing oxygen delivery to brain tissue In a prospective trial of severely brain injured adults randomized to prophylactic hyperventilation or normocapnic treatment, the patients in the hyperventilation group had a significantly worse outcome [75] However, based upon the lack of definitive evidence, the current consensus guidelines recommend against prophylactic severe hypoventilation [26] and further suggest that mild hyperventilation (PaCO2 30–35 mmHg) may be considered for intracranial hypertension refractory to sedation, CSF drainage, and hyperosmolar therapy, only if advanced neuromonitoring methods are used to avoid cerebral ischemia Temperature Control Hyperthermia after TBI has been correlated with worse injury and functional outcome in both animal models and clinical studies in adults The mechanisms of damage include worsening of the secondary insult by increasing cerebral metabolic demands, damage by excitotoxicity, and cell death by stimulation of apoptotic pathways Therefore hyperthermia should be aggressively avoided in children with TBI The basis for the use of hypothermia (core body temperature