Both primary and secondary injuries are described in pediatric patients with head trauma, and the presence of these injuries affects outcome.
In a prospective, multicenter study of 43,399 pediatric patients treated for head injuries in US emergency rooms, Quayle et al found that the most common mechanisms of injury in the overall population were the following [5] :
Falls from any distance (27%)
Falls while standing, walking, or running (11%)
Collisions with a stationary object when walking or running (6%)
Motor vehicle crashes (9%)
Bicycle crashes (4%)
Falls were the most frequent cause of traumatic brain injury (TBI) for children under age 12, whereas assaults, motor vehicle accidents, and sports activities were the most frequent cause of injuries for adolescents. Overall, 98% of head injuries were classified as mild.
A large proportion of injuries caused by motor vehicle or bicycle crashes occurred when the child was not using a seat belt (36%) or a helmet (72%). [5] Among the 16% of patients in a motor vehicle crash who were diagnosed with a TBI, 52% were not using a seat belt. Of the 4% of bicycle crash patients with a TBI, 93% were not wearing a helmet.
Among the 37% of children who underwent cranial computed tomography (CT) scanning, TBIs were identified in 7%, and 3% had skull fractures without intracranial findings. The most common injury identified on CT scan was subdural hematoma, followed by subarachnoid hemorrhage and cerebral contusion.
Primary injuriesThe primary injury occurs at the time of impact, either via direct injury to the brain parenchyma or via injury to the long white-matter tracts through acceleration-deceleration forces. [6]
Direct injury to the brain parenchyma occurs as the brain makes forceful contact with the bony protuberances of the calvaria or is penetrated by bony fragments or a foreign body. Impact on the brain at the time of the insult results in a coup injury, whereas contrecoup injury occurs as the brain is forced against the bony protuberances opposite the point of the impact.
Intracranial hemorrhage (ICH) may also result from shearing or laceration of vascular structures. Although exceptions occur, epidural hematomas are usually secondary to arterial injury, while subdural hematomas are usually secondary to venous injury. Because of the higher arterial blood pressure, epidural hematomas may enlarge very rapidly, while subdural hematomas generally develop more gradually. However, subdural hematomas are typically associated with underlying direct tissue injury, which is less common with epidural hematomas.
Acceleration-deceleration forces cause shearing of the long white-matter tracts, leading to axonal disruption and secondary cell death.
Secondary injuriesThe secondary injury is represented by systemic and intracranial events that occur in response to the primary injury and further contribute to neuronal damage and cell death. [6]
The systemic events are hypotension, hypoxia, and hypercapnia and may occur either as a direct result of primary injury to the central nervous system (CNS) or as a consequence of associated injuries in a person with multiple traumas. Because of many factors (eg, higher brain metabolic activity, limited substrate availability, delay in seeking care), secondary brain injury commonly leads to greater morbidity than primary injury, while the reverse is true in adults.
The intracranial events are a series of inflammatory changes and pathophysiologic perturbations that occur immediately after the primary injury and continue over time. The nature of these events is poorly understood but has received greater attention due to the impact of secondary injury in pediatric traumatic brain injury.
Inflammatory changes are the result of a cascade of biomolecular alterations triggered by the initial insult, leading to microcirculatory disruption and neuronal disintegration. A series of factors such as free radicals, free iron, and excitatory neurotransmitters (glutamate, aspartate) are the result of these inflammatory events, and their presence contributes to negative outcomes. These pathophysiologic events include cerebral edema, increased ICP, hyperemia, and ischemia. Apoptotic neuronal cell death is more prevalent than necrotic neuronal cell death in pediatric patients, likely secondary to the role that apoptosis plays in the development of the pediatric brain.
Altered autoregulation of cerebral blood flowBecause the brain has minimal ability to store energy, it depends primarily on aerobic metabolism. The delivery of oxygen and metabolic substrate to the brain is maintained by a constant supply of blood, referred to as cerebral blood flow (CBF). CBF, defined as the amount of blood in transit through the brain at any given point in time, is estimated to be 50 mL/100 g/min in a healthy adult and is known to be much higher in children. However, the minimum amount necessary to prevent ischemic injury remains unknown.
CBF is influenced by mean arterial blood pressure (MAP), ICP, blood viscosity, metabolic products, and brain vessel diameter. CBF should not be confused with cerebral blood volume (CBV), which represents the amount of blood present in the brain vasculature. Because brain tissue and CSF volumes remain relatively stable, acute changes in CBV are mostly responsible for acute changes in ICP. CBV depends primarily on the diameter of intracranial vessels, so therapeutic interventions to reduce intracranial blood vessel diameter (vasoconstriction) are the most effective methods to acutely reduce elevated ICP. Hyperventilation, in the acute phase, decreases ICP by decreasing CBV via alkalosis-induced cerebral vasoconstriction.
The brain maintains constant blood flow through a mechanism known as autoregulation. This process occurs over a wide range of blood pressures through changes in cerebral resistance in response to fluctuations in MAP pressure. At a MAP of 60-150 mm Hg, CBF is maintained. At 60 mm Hg, the cerebral vasculature is maximally dilated. At 150 mm Hg, it is maximally constricted. (These are adult ranges; pediatric ranges are unknown but are likely age-dependent.) Fluctuations of MAP beyond either end of this range lead to alterations in CBF and contribute to ischemia or disruption of the blood-brain barrier.
Several mechanisms are known to affect autoregulation of CBF; they may be divided into the following categories:
Metabolic products
Arterial blood gas content
Myogenic factors
Neurogenic factors
Endothelium-dependent factors
The effects of these mechanisms are not fully known, and their mechanism of action is still under experimental investigation.
CBF is closely linked to cerebral metabolism. Although the mechanism of coupling is not clearly defined, it is thought to involve vasodilators released from neurons. Several factors have been implicated, such as adenosine and free radicals. Pathophysiologic states that are known to increase metabolic activity (eg, fever and seizure activity) lead to an increase in CBF.
CBF can be altered by changes in the partial pressure of oxygen or carbon dioxide. Alteration in the partial pressure of oxygen acts on the vascular smooth muscle through mechanisms that remain unclear. Hypoxia causes vasodilatation with significant increase in CBF. Increases in oxygen pressure result in dose-dependent vasoconstriction, although to a less pronounced degree than hypoxia-induced vasodilation.
Hypercarbia increases CBF up to 350% of normal, while hypocapnia produces a decrease in blood flow. The mechanism appears to involve alteration in tissue pH that leads to changes in arteriolar diameter. This mechanism is preserved even when autoregulation is lost. However, renal compensation for respiratory alkalosis causes tissue pH levels to normalize, restoring CBF, which limits the effectiveness of prolonged hyperventilation for control of elevated ICP.
The myogenic mechanism was long considered to be the most important in the autoregulation process. Changes in the actin-myosin complex were thought to lead to rapid changes in the vasculature diameter, thus affecting the CBF. It has now been shown that changes in the actin-myosin complex mostly cause dampening of arterial pulsation and have little direct effect on cerebral autoregulation.
The neurogenic mechanism is represented by the effect of the sympathetic system on the cerebral vasculature. The sympathetic nervous system shifts autoregulation toward higher pressures, whereas sympathetic blockade shifts it downward.
Studies have identified nitric oxide (NO) as one of the factors affecting cerebral autoregulation; it does so by producing relaxation of cerebral vessels. NO is present in several conditions, such as ischemia, hypoxia, and stroke. It is generated by different cells at rest but also under direct stimulation by factors such as cytokines.
Alterations in CBF during periods of hyperoxia, hypoxia, hypercarbia, and hypocarbia occur due to changes in local NO production. Vasodilation from somatosensory stimulation occurs through changes in neurogenic NO production, and impaired vasodilation associated with endothelial dysfunction appears to be due (at least in part) to the production of reactive oxygen species and reduced NO bioavailability. [7]
TBI may lead to loss of autoregulation through alteration of any of these mechanisms. One study found that mild TBIs are more likely than orthopedic injuries to cause transient or persistent increases in postconcussive symptoms during the first year after injury. [8] These mechanisms represent the foundation on which the medical management of increased ICP and cerebral perfusion pressure (CPP) is based in patients with TBI.
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