Emergency Treatment Options for Pediatric Traumatic Brain Injury

J Exo; C Smith; R Smith; MJ Bell


Pediatr Health. 2009;3(6):533-541. 

In This Article

Abstract and Introduction


Traumatic brain injury is a leading killer of children and is a major public health problem around the world. Using general principles of neurocritical care, various treatment strategies have been developed to attempt to restore homeostasis to the brain and allow brain healing, including mechanical factors, cerebrospinal fluid diversion, hyperventilation, hyperosmolar therapies, barbiturates and hypothermia. Careful application of these therapies, normally in a step-wise fashion as intracranial injuries evolve, is necessary in order to attain maximal neurological outcome for these children. It is hopeful that new therapies, such as early hypothermia or others currently in preclinical trials, will ultimately improve outcome and quality of life for children after traumatic brain injury.


Traumatic brain injury (TBI) is the leading killer of children in the USA after the first year of life. Based on 2005 data from the CDC, trauma was the leading cause of death in every pediatric age group except for those under 1 year of age (where it was fourth), and traumatic brain injury is thought to be responsible for more than 50% of all traumatic deaths in children.[1] Between 100,000 and 150,000 children suffer from severe TBI and approximately 10–15% result in death or severe disability.[2] The burden of childhood TBI is expected to exceed US$ 30 billion annually within the USA and this estimate is only likely to grow as survivors continue to utilize resources with improvements in rehabilitation and outpatient care.[3,4] Despite this enormous burden to society, brain-specific therapies for TBI are relatively limited.

In order to understand therapies for TBI, a basic understanding of the pathogenesis of brain injury after trauma is required. TBI consists of the primary injury followed by an evolution of injury and potential secondary insults. Primary injury is the damage inflicted at the time of the traumatic event and consists of contusions to brain parenchyma, lacerations of brain substance, which can lead to hematomas (epidural and subdural) and hemorrhages (intraparenchymal and subarachnoid), white matter damage (such as diffuse axonal injury) and other damage to bony structures or blood vessels. Except for removal of extra-axial blood collections that may be compressing the brain parenchyma, there are no current treatments for these primary injuries. The evolution of TBI involves the body's reaction to injury and begins within hours after the injury is sustained. In this early time period, cerebral blood flow (CBF) is often lower than normal in children and may be inadequate to sustain normal neurological functioning in some brain regions. Direct injury to brain tissue can lead to edema formation as intravascular fluid traverses the damaged blood–brain barrier or intracellular pathways are activated that lead to cell swelling and cell death. Secondary factors such as systemic hypoxia, hypotension, hyperpyrexia and hyperglycemia can lead to exacerbation of injury and less favorable neurological outcome. Precise assessments and determination of thresholds of these events that may lead to adverse outcome are largely unknown for children after TBI, yet remain an intense focus of research at the current time.

Treatment strategies for TBI in children are largely based on a few key physiological principles: the Munro–Kellie doctrine; cerebral blood pressure autoregulation; and the relationship between metabolic demands and blood flow (Figure 1). Over 100 years ago, Munro and Kellie recognized the relationship between the contents and volume of the intracranial compartment. This doctrine states that the volume of the intracranial contents (brain, cerebrospinal fluid [CSF], arterial and venous blood and any pathological mass) are related to the pressure within the relatively rigid encasement of the skull. As pathological masses accumulate in the cranial vault and after compensatory mechanisms (expansion of cranial sutures, increased CSF absorption and extrusion of venous blood into the thorax) are overcome, further increases in intracranial volume lead to critical increases in intracranial pressure (ICP). These increases in ICP, generally termed intracranial hypertension when ICP is greater than 20 mmHg, eventually lead to decreased arterial blood volume, decreased cerebral blood flow, brain ischemia and ultimately cerebral herniation if untreated. A second key neurocritical care principle is CBF autoregulation. Normally, CBF remains constant over a relatively wide range of mean arterial pressures (MAP), with maximal vasodilation of arteries in the lower limit of autoregulatory range (generally MAP ~50 mmHg in adults) and maximal vasoconstriction at the upper limit (MAP ~150 mmHg). Manipulations of the constriction/relaxation of cerebral arterioles can have profound effects on ICP as maximally vasodilated blood vessels within the brain will lead to increased cerebral blood volume. Lastly, cerebral metabolism, as measured by either oxygen or glucose consumption, is tightly correlated with CBF demands in normal conditions. Therefore, as metabolism is decreased by medications or decreased cerebral function, blood flow requirements will be decreased. Conversely, as metabolism is increased, CBF requirements are increased.

Figure 1.

The Munro–Kellie Doctrine explains the relationship between intracranial volumes and intracranial pressure in physiological and pathophysiological conditions. The volume of the intracranial vault (the area represented by the rectangle) is generally fixed in adults and most children. The contents of the intracranial vault in the normal condition include the brain, arterial blood, venous blood and CSF, and are maintained at a relatively low ICP (Panel 1; normal). After an injury, swelling/edema/pathological tissue can increase within the brain (Panel 2; compensated). Compensatory mechanisms, including increased CSF absorption, extrusion of CSF into the spinal canal and extrusion of venous blood into the thorax, initially limit any changes in ICP. When these compensatory changes are exhausted (Panel 3; uncompensated), any further increases in intracranial volumes are associated with concomitant increases in ICP that eventually can compromise arterial blood flow, ultimately leading to cerebral herniation. CSF: Cerebrospinal fluid; ICP: Intracranial pressure.

To a great extent, all current and future therapies for TBI in children can be understood by these principles, as we outline below. The hallmarks of the currently recommended treatment strategies for severe TBI are aimed at normalizing physiologic parameters and limiting secondary injury to the brain. In doing so, steps must be taken to optimize oxygen and glucose delivery to the brain and then brain-specific therapies need to be applied in a rational manner to maximize benefits and minimize side effects of treatment. The following sections generally outline therapies with the fewest side effects first (mechanical and CSF drainage) with increasing side effects toward the end of this section (barbiturates and hypothermia). Guidelines for the management of severe TBI in children have been formulated to synthesize the best evidence to date regarding many aspects of care[5] and they are currently under revision. This manuscript will describe the physiological basis for these therapies and summarize the evidence that support their use.


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