Head Injury and Facial Trauma

Head Injury

Traumatic brain injury (TBI) is an important cause of injury-related death and disability in children.¹ In the USA, there are an estimated 1.7 million people with TBI annually, with a reported 52,000 deaths and 275,000 hospitalizations. Children ages 0 to 4 years and 15 to 19 years are most likely to suffer TBI. Nearly half a million emergency department visits annually are for children less than 14 years with TBI. Males, age 0 to 4 years, have the highest rates of TBI-related emergency department visits, hospitalizations, and deaths combined.²

Head trauma from child abuse remains a significant concern. In children younger than age 1 year, nonaccidental trauma (NAT) is the most common cause of fatal TBI.3,4 Head trauma associated with NAT has a higher rate of subdural hematomas, subarachnoid hemorrhages, and retinal hemorrhages when compared with nonabusive head trauma. Public health campaigns have brought attention to the dangers of shaking a young child and have provided resources for parents and caretakers who may be at risk of harming a child.⁵

Although the reasons are not entirely clear, there has been a general trend in improved outcomes after severe TBI in children.⁶ The decline in morbidity and mortality are likely due to improved prehospital care, regionalization of pediatric trauma care, adherence to evidence-based practice guidelines, more aggressive care (such as intracranial pressure [ICP] monitoring and early surgical evacuation of mass lesions), improved diagnostic imaging (computed tomography [CT], magnetic resonance imaging [MRI]), and advances in intensive care. In January 2012, the second edition of evidence-based practice guidelines was published for the acute medical management of severe TBI in infants, children, and adolescents.⁷ These guidelines have allowed a decrease in variability in care across centers, but there is a striking lack of data from well-designed, randomized controlled trials.

Brain Injury Mechanisms

The Monro–Kellie doctrine is an important concept relating to the understanding of ICP dynamics (Fig. 17-1). The Monro–Kellie doctrine uses a simple hydraulic approach to the cerebral circulation. Given that the cranium is a rigid, nonexpansile container, it states that the total volume of the intracranial contents must remain constant and any increase in the volume of one component must be at the expense of the others, assuming the intracranial volume remains constant. Thus, very early after injury, a mass such as an expanding hematoma may be enlarging while the ICP remains normal. Once the limit of displacement of CSF and intravascular blood has been reached, ICP rapidly increases (Fig. 17-2). Further work has shown that the relationship between ICP and cerebral blood flow (CBF) is much more complex and variable. Whereas simultaneous measurement of ICP and CBF would be most helpful in optimizing therapeutic strategies, the Monro–Kellie doctrine provides a reasonable basic explanation of intracranial dynamics.

FIGURE 17-1 Monro–Kellie doctrine. The Monro–Kellie doctrine states that the cranial compartment is incompressible and that the volume inside the cranium is a fixed volume. The cranium and its constituents (blood, cerebrospinal fluid [CSF], and brain tissue) create a state of volume equilibrium such that any increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another.

FIGURE 17-2 Intracranial pressure (ICP)–volume relationship. Small increases in brain volume do not lead to immediate increase in ICP because of the ability of the cerebrospinal fluid to be displaced into the spinal canal as well as the ability the falx cerebri to stretch slightly between the hemispheres and the tentorium between the hemispheres and the cerebellum. However, once the ICP has reached around 25 mmHg, small increases in brain volume can lead to marked elevations in ICP.

CBF is defined as the velocity of blood through the cerebral circulation. In adults, the normal CBF is 50–55 mL/100g of brain tissue/minute. In children, CBF may be much higher depending on their age. At 1 year of age, it approximates adult levels, but at 5 years of age, normal CBF is approximately 90 mL/100 g/min and then gradually declines to adult levels by the mid-late teens. Brain injury severe enough to cause coma can result in a 50% reduction in CBF during the first 6 to 12 hours after injury.10,11 It usually increases over the next 2 to 3 days, but for those patients who remain comatose, CBF remains below normal for days or weeks after injury. There is increasing evidence that such low levels of CBF are inadequate to meet the metabolic demands of the brain early after injury and that regional, if not global, cerebral ischemia results.^12–14

Cerebral perfusion pressure (CPP) is the differential pressure of arterial flow into and venous flow out of the brain. CPP may be defined by the difference between mean arterial pressure (MAP) and ICP. CPP is considered the transmural pressure gradient that is ultimately the driving force required for supplying cerebral metabolic needs. As ICP increases following head injury, CPP decreases and blood flow to the brain eventually declines. At a CPP of 10 mmHg, blood vessels collapse and blood flow ceases.

Current techniques available to measure CBF, such as transcranial Doppler and Xenon-enhanced CT imaging, are still considered experimental in the management of severe TBI. Because CPP is easily determined by ICP monitoring, it has become a critical parameter for defining treatment options. Studies have shown a good correlation between CPP and CBF in patients with intact cerebral autoregulation.¹³ However, cerebral autoregulation is often disrupted after severe TBI and measures of cerebral vascular resistance may be more useful in guiding therapy.^15,16

Cerebral autoregulation refers to a homeostatic process that allows CBF to remain constant over a wide range of MAPs. Arterial vessels can dilate or constrict in response to various physiologic changes, including ICP and systemic arterial pressure, to maintain normal flow and normal brain metabolism. In healthy adult patients, CBF remains constant with a MAP between 60–160 mmHg, or a CPP between 50–150 mmHg.¹⁷ Normally, with elevated systemic blood pressure, reflexive vasoconstriction will occur to prevent intracranial hypertension. In contrast, a moderate decrease in systemic blood pressure will paradoxically result in increased ICP because compensatory reflex vasodilatation will occur. When perfusion pressure falls below 50 mmHg, cerebral ischemia develops and compensatory cerebral arteriole vasodilatation is exhausted. When perfusion pressure exceeds 150 mmHg, cerebral arteriolar impedance is overcome, the affected vessels passively dilate, and fluid is forced through a damaged endothelium into the brain, causing diffuse vasogenic edema. Impaired cerebral autoregulation after TBI and age-related changes in CBF make the immature brain susceptible to secondary injury, both from diminished and excess CBF, and are both associated with a poor neurologic outcome.¹⁸

Historically, treatment protocols were principally directed toward reducing ICP. Hyperventilation and fluid restriction were important components in these older protocols. Sustained elevations in ICP above 20 mmHg are poorly tolerated by the injured brain and have been associated with poor neurologic outcome and increased mortality in pediatric patients.¹⁹ Sustained elevation in ICP may result in cerebral ischemia if cerebral perfusion is impaired, and ultimately may result in cerebral herniation. Current treatment strategies seek to optimize CPP while reducing ICP, with little reliance on hyperventilation or fluid restriction. CPP is likely an age-related continuum, thus making it problematic to develop treatment protocols based on a single number for all age groups. To date, no study has demonstrated that active maintenance of CPP above any target threshold in infants and children following TBI improves mortality or morbidity. However, there seems to be a threshold of less than 40 mmHg that is associated with increased mortality; therefore, most treatment guidelines recommend a minimum CPP of 40 mmHg.

Primary Brain Injury

Primary brain injury occurs as a result of direct injury to the brain parenchyma due to shear forces at the time of impact. Both cortical disruption and axonal injury can occur, resulting in a cascade of events contributing to secondary brain injury, which will be discussed later. Cortical disruption, if occurring within minutes to hours, is not likely to be amenable to resuscitation.

Skull fractures occur commonly with head injury and are readily diagnosed with CT. In children, a skull fracture should prompt an evaluation of the underlying brain parenchyma given the significant impact it takes to injure the skull. Fractures of the skull vault can occur in either a linear or a stellate fashion. Fractures involving the skull base are typically associated with a greater force than simple cranial vault fractures. The classic signs of basilar skull fractures include Battle’s sign (ecchymoses over the mastoid process associated with an ipsilateral skull fracture), raccoon eyes and CSF rhinorrhea (associated with a cribriform plate fracture), and otorrhea (associated with fracture of the mastoid air cells or temporal bone fracture). Meningitis associated with a basilar skull fracture occurs in up to 10% of patients.²⁰ Despite the risk of infection, the routine use of prophylactic antibiotics is not recommended as they have not been shown to prevent meningitis from occurring, and tend to select out for resistant organisms.^21–23 Vaccination against Streptococcus pneumoniae should be considered for all patients with a basilar skull fracture and CSF leak due to the increased risk of pneumococcal-associated meningitis.²⁴

Post-traumatic intracranial hemorrhage includes epidural hematomas, subdural hematomas, and subarachnoid hemorrhages. Epidural hematomas usually occur in the middle fossa and are often associated with an injury to the middle meningeal artery, although they can occur in the anterior or posterior fossa. The classic CT description is a lenticular hematoma, bound by suture lines, because of the tightly bound dura (Fig. 17-3). Clot formation under the calvaria compresses the dura and can cause rapid neurologic deterioration as the brain becomes further displaced. Skull fractures overlying the epidural hematoma are common. The classic presentation of a patient with a lucid interval followed by clinical deterioration is rare in children. Only after the hematoma enlarges is clinical evidence of elevated ICP noted. Typical symptoms include headache, lethargy, emesis, irritability, confusion, and decreased level of consciousness. Progressive deterioration results in seizures, changes in vital signs with hypertension and respiratory instability, pupillary changes, posturing, and cardiovascular compromise. Prompt neurosurgical evacuation is imperative for patient survival and good outcome. Evacuation of extremely large clots (>40 mL) in children often results in very good long-term results, provided that operative intervention is timely.

FIGURE 17-3 CT scan shows an epidural hematoma (asterisk) in a 14-year-old patient. (Courtesy of Dr Lisa Lowe.)

Subdural hemorrhages are classified as acute (<3 days old), subacute (3-10 days old), and chronic (>10 days old). Acute and subacute subdural hemorrhages are not infrequent in infants, and often the result of birth injury or NAT (Fig. 17-4). They usually result from lacerated bridging veins, or from associated contusions hemorrhaging into the subdural space. The superficial cortical veins in small children lack any reinforcement from arachnoidal trabeculae and are susceptible to inertial loading. Subdural hematomas tend to follow the convexities of the brain and cover the entire hemisphere. The cranial CT demonstrates hyperdense crescent-shaped blood collections at the surface of the brain, often associated with mass effect and cortical edema. Occasionally, and particularly when anemia is present, the CT findings of an acute subdural hematoma may have an isodense appearance that belies the actual hemorrhagic character later found at the time of operation.

FIGURE 17-4 Hyperacute subdural bleeding (arrow) is seen on this cranial CT scan of a 9-month-old patient. (Courtesy of Dr Lisa Lowe.)

Acute subdural hemorrhages are usually associated with a worse prognosis than patients with an epidural hematoma, primarily related to the underlying brain damage. Operation is indicated when neurologic deterioration occurs as a result of the combined effect of the subdural hemorrhage and parenchymal injury, either from the compressive effect of the subdural blood or from the combined effect of impact forces on the entire cerebrum and diffuse bleeding. In infants, it is possible to tap the subdural space at the level of the fontanelle and produce rapid decompression. Large subdural hematomas with significant mass effect require more extensive craniotomies.

Subacute subdural hematomas in the context of trauma are much less frequent in the pediatric population. However, they will be seen in emergency settings when they are a cause of neurologic problems, and when they are considered a manifestation of previous or recurrent NAT. As with acute hematomas, subacute subdural hematomas will have a nonspecific presentation. Affected children have both the symptoms of increased ICP (coma, irritability, lethargy, emesis, seizures) and the signs of elevated ICP (frontal bossing, enlarged heads, dilated scalp veins, sun-setting eyes, papilledema, and bulging fontanelles). The CT scan often shows isodense or hypodense fluid collections at the cerebral convexities. MRI studies are helpful for making the diagnosis of these bleeding events. As with acute subdural hematomas, operative evacuation is often necessary.

Chronic subdural hematomas can cause symptomatic elevation of the ICP and may require interventions to manage cranial growth and CSF pressure. Patients present with symptoms similar to those of a subacute subdural hematoma. Management options include serial percutaneous drainage, limited craniotomies to drain and irrigate the subdural space, and subdural/peritoneal shunts.

Subarachnoid hemorrhage (SAH) in acutely traumatized children is common and is rarely the result of aneurysmal bleeding (Fig. 17-5). Subarachnoid bleeding occurs from disruption of the fragile pia-arachnoidal vasculature. This often occurs over the convexities of the brain affected by coup type injuries or the frontotemporal poles affected by contrecoup injuries. Traumatic SAH can also occur in the interhemispheric fissure and in the basilar cisterns. When SAH is an isolated finding following minor trauma, no specific therapy is indicated except symptomatic amelioration of chemical meningitis, meningismus, and photophobia. SAH can result in hydrocephalus and may require ventricular shunting to relieve the increased ICP. In patients with severe TBI, SAH is associated with a poor outcome and may also be associated with cerebral vasospasm. Transcranial Doppler imaging can be utilized to identify vasospasm. Therapy for vasospasm in adults include calcium channel blockers and neurointerventional techniques; however, these are not well studied in children and not commonly used.25,26

FIGURE 17-5 Subarachnoid hemorrhage (arrows) is present on this cranial CT scan of a 10-year-old patient. (Courtesy of Dr Lisa Lowe.)

Secondary Brain Injury

The cornerstone of TBI management is the prevention of secondary injuries. Secondary brain injury includes both the evolution of damage within the brain related to a cascade of macroscopic and microscopic events, and the effects of secondary insults, including hypoxia and hypotension. Endogenous secondary brain injury involves the macroscopic cascade of edema, ischemia, necrosis, elevated ICP, and inadequate CPP.

Brain swelling traditionally has been described as either vasogenic or cytotoxic. The time course of brain edema is variable. It is thought, however, that vasogenic edema occurs early after injury and cytotoxic edema occurs in a more delayed fashion. Vasogenic swelling results from the disruption of the blood–brain barrier. The blood–brain barrier is maintained by tight junctions between endothelial cells that line the vessels of the brain. Injury to these cells allows extravasation of fluid and proteins into the interstitial space of the brain parenchyma. Disruption of these cells can occur from the primary injury or from free radical formation, cytokines, and other secondary mechanisms of brain injury. Cytotoxic edema is edema of the cells themselves, resulting from a failure of cellular ion homeostasis and membrane function.

Edema of the brain is an important marker for injury and is also a cause of secondary injury. In early (<24 hours) fatal closed-head injuries in children, CT scans often demonstrate little or no significant parenchymal bleeding. However, in children, rapid development of edema is commonly seen on serial CT scans and the diffuse brain swelling causes the obliteration of the ventricles and loss of the basilar cisterns and subarachnoid space. As swelling progresses and the compensatory mechanisms of the brain are exhausted, ICP increases markedly with small changes in intracranial volume (see Fig. 17-2). Cerebral edema typically develops early after injury, peaking at 72 to 96 hours, and then gradually resolves over the next week in survivors.²⁷

Studies in adults utilizing xenon CT have shown a reduction in CBF early after severe TBI.10,12 This hypoperfusion may be further exacerbated by hypotension and hypoxia. It is clear that this early hypoperfusion or ischemia after severe TBI is associated with a poor outcome.^28,29 Proposed mediators involved in early post-traumatic ischemia include direct vascular disruption, production of endothelin-1 (a potent vasoconstrictor), loss of endogenous vasodilators (endogenous nitric oxide synthase), and likely many other complex, interrelated, cellular and metabolic events.

The release of excitatory amino acids, such as glutamate, results in neuronal injury after TBI. Glutamate is the most abundant neurotransmitter in the brain. However, toxic levels cause neuronal cell death.30,31 After TBI, glutamate and other excitatory amino acids are released, resulting in neuronal swelling, calcium influx, and release of cytotoxic enzymes leading to cell death. Studies have failed to demonstrate efficacy of anti-excitotoxic therapies, perhaps owing to their application in all patients with TBI rather than those with excitotoxicity, and because treatment may have been initiated too late.³²

Oxidative stress with free radical formation is an important mechanism leading to secondary injury. Free radicals damage endothelial cells and injure the brain parenchyma. This results in disruption of the blood-brain barrier and resultant vasogenic and cytotoxic edema. Free radical scavengers, such as vitamin E, ascorbic acid, and superoxide dismutase, attempt to minimize injury by binding with the free radicals. However, these mechanisms often become overwhelmed and the process becomes self-perpetuating. Clinical studies are ongoing to identify pharmacologic free radical scavenging agents.

Apoptosis requires a cascade of intracellular events for completion of cell death and is thus termed programmed cell death. Calcium influx into the cell, oxidative stress, and energy depletion all appear to be important intracellular triggers of apoptosis. As our understanding of the complex biochemical, cellular, and molecular responses to TBI progresses, application of therapeutic strategies and agents may help halt the secondary injury processes.