Head Trauma

Chapter 99


Head Trauma image



Head injury occurs every 7 seconds in the United States, resulting in approximately one death every 5 minutes. It is the leading cause of death among persons under the age of 24 years. Approximately 200,000 patients die or are permanently disabled each year from brain trauma. Sixty percent of traumatic brain injuries (TBIs) are caused by road traffic accidents, 20% to 30% are caused by falls, approximately 10% are caused by violence, and another 10% are due to work- or sports-related injuries. Globally, the burden caused by TBI to patients, caregivers, and society is large and increasing.



Classification of Head Trauma



Scalp Injury


The head is a multilayered structure composed of the scalp, skull, dura, and brain. The degree to which each layer can withstand injury depends on its tissue composition and relative perfusion. The first layer of brain protection is the scalp. Because the scalp is a highly vascular structure, large scalp lacerations can result in enough blood loss to cause hypovolemic shock. Violation of the scalp with concomitant injury to the skull and dura can lead to intracranial infection. image


Irrigation, local debridement, and primary closure are the initial steps of treatment for lacerations. In cases of scalp avulsion with moderate to severe scalp loss, rotational flaps, skin grafting, microsurgical reimplantation, or free tissue transfers may be required. The process of tissue expansion has greatly enhanced scalp reconstruction. Implantation of a subcutaneous silicon reservoir, followed by serial injections of sterile saline into the reservoir over several weeks, can sufficiently stretch the scalp skin for flapping purposes. Up to 50% of the scalp can be replaced with this method.



Skull Injury


When the force sustained by the skull is greater than the strength of the skull, the skull fractures. Cranial vault fractures can be classified as open or closed, depending on the integrity of the overlying scalp and underlying dura. Among the various types of fractures, the linear fracture is the most common. A simple linear fracture with no scalp violation may only require brief observation to rule out intracranial injury. If the fracture violates perinasal air cavities, however, the risk of cerebrospinal fluid (CSF) rhinorrhea or otorrhea increases; meningitis can also develop when the fracture exposes the epidural space to sinus contents. Such fractures may require surgical intervention. Finally, injury to vascular structures, such as the middle meningeal artery or venous sinuses, can complicate skull fractures and result in potentially lethal epidural hematomas or sinus thromboses.


Depressed fractures result from impact with small surface area objects (< 2 square inches) at high velocities. They may be open or closed and frequently involve vascular structures. If the injury violates both dura and cortex, there may be significant evolution of hematoma and there exists the potential for intracranial contamination from bone fragments, foreign bodies, or both. The management of depressed skull fractures is controversial. image


From a series of 284 patients with depressed fractures, only 2.8% of those treated nonoperatively developed infectious complications. From those data, investigators concluded that the majority of these fractures are best treated conservatively. The following fractures and associated injuries typically require surgical management: gross contamination or established infection, presence of CSF or brain tissue in the wound, a concomitant intracranial lesion requiring surgery, severe bleeding from the wound, frontal sinus involvement, cosmetically unacceptable depressions, and severely comminuted fractures.


Whereas larger fractures within the skull base are usually readily apparent on computed tomography (CT) imaging, smaller fractures are frequently absent on plain film imaging and can be easily missed with CT. If the suspicion for basilar skull fracture remains high despite negative radiographic findings, the diagnosis can still be made on clinical grounds.


The thin anterior base of the skull is particularly susceptible to injury. The presence of “raccoon’s eyes” (periorbital ecchymoses) or Battle’s sign (retromastoid hematoma) reliably signifies a skull base fracture. CSF otorrhea or rhinorrhea, hemotympanum, or blood in the external auditory meatus without evidence of direct ear trauma is also a hallmark of these fractures. Skull base fractures can involve the carotid canal and result in carotid rupture, dissection, or thrombosis. When this is suspected, cerebral angiography is indicated to evaluate vessel integrity. image


Fractures through any of the skull base foramina can cause specific cranial nerve injuries. The delicate neurons of the olfactory nerves that pass through the cribriform plate are especially prone to disruption. As with the linear fractures, operative repair is usually not indicated for skull base fractures unless there is persistence of CSF leak or compromise of vascular or neural tissue. Pulsatile exophthalmos, ophthalmoplegia, chemosis, or a bruit with visual loss should alert the examiner to a possible carotid-cavernous sinus fistula, which may require immediate endovascular or, rarely, operative treatment.




Meningeal Injury


Injury or violation of the meninges rarely occurs without violation of the skull. Bridging veins from the pial surface of the brain to the dura and its venous structures are easily torn, resulting in subdural hematoma formation. As discussed earlier, violation of the dura, particularly at the cranial base, may include vascular structures or lead to CSF rhinorrhea or otorrhea.


About 5% of epidural hematomas occur in the posterior fossa. Because of the limited volume within this space in addition to its close proximity to the brain stem, treatment of any expanding lesion in the posterior fossa must be considered urgent. Bounded posteriorly and laterally by bone and superiorly by the tentorium cerebelli, expanding posterior fossa hematomas can rapidly cause tonsillar herniation and brain stem compression leading to coma and death.


This occurrence was confirmed in a landmark study by Seelig and colleagues, who reported that patients who underwent craniotomy and evacuation of subdural hematomas within 4 hours of injury had a significantly lower mortality rate than did those who received treatment after the 4-hour window (30% versus 90% mortality).




Brain Injury



Focal Brain Injuries


The neurologic presentation of focal brain injury relates directly to the specific region of the brain involved. Global neurologic deficits or coma with focal injuries are usually the result of brain stem compression and require urgent diagnosis and treatment.


In a study of 1448 patients with mild head injury (defined as a Glasgow Coma Scale [GCS] score of 13 to 15; imageTable 99.E1), the most common lesion was a contusion. Contusions often involve the surface of the brain beneath vault fractures, at points where brain the surface collides with bony surfaces of the middle and frontal fossa, or in regions of the cortex where high surface strains are produced by the inner table of the skull. This occurs most commonly in the frontal and temporal lobes but may occur at any site including the brain stem and cerebellum. In patients with focal injuries, the presence of contusion alone tends to portend a good prognosis. Intracerebral hematomas result from torn blood vessels in deeper brain structures. They are not contiguous with the cortical surface and typically occur in the deep white matter of the frontal and temporal lobes. Injuries in which the pial surface is violated with parenchymal disruption are termed cerebral lacerations.


Epidural hematomas result from injuries that cause disruption of dural vessels, sinuses, or diploic channels, allowing blood to dissect into the epidural space. The middle meningeal artery is frequently injured with temporal bone trauma, resulting in an epidural hematoma.


Epidural hematomas can occur in the setting of a relatively minor head injury and may present with only minor neurologic signs or symptoms. Although they occur in less than 3% of head-injured patients, it is important to have a high index of suspicion because rapid expansion, if not treated immediately, can cause brain compression. Prognosis with epidural hematomas is related to age, GCS at presentation, and the timing of evacuation. Concomitant intracranial injury, such as subdural hematoma, adversely affects outcome. image


Subdural hematomas are focal lesions that result from contact or acceleration and inertial forces. When vascular structures of the pial surface are disrupted, bleeding occurs within the subdural space. When the head undergoes rapid deceleration, as in a motor vehicle accident, cortical bridging veins can tear and bleed into the subdural space. In general, subdural hematomas have a poor prognosis because, in contrast to epidural hematomas, they are usually accompanied by a significant parenchymal injury. The morbidity and mortality associated with subdural hematomas are related to the GCS on presentation, age, intracranial pressure (ICP), and mechanism of injury. An evolving hematoma may cause herniation and brain stem compression leading to a decreased level of consciousness. Rapid recognition of this process and immediate treatment are essential. image



Diffuse Brain Injury


Concussion and diffuse axonal injury represent two ends on the spectrum of diffuse brain injury. Typically with diffuse brain injury there are no grossly evident intracranial lesions. As a result, alterations in level of consciousness result from global or diffuse disruption of the anatomic and physiologic neural substrates rather than brain stem compression. The perturbation lies at the level of the neuronal cell membranes and axolemmas and can be widespread in both the cerebrum and brain stem.


Concussion is a mild form of global neurologic dysfunction. The exact mechanism and pathophysiology of concussion remain an enigma. The neurologic disturbances seen in concussive syndromes may relate to the magnitude and site of head injury. Although concussion may or may not be associated with loss of consciousness, amnestic periods and long-term higher cognitive deficits have been reported. In classic concussions (i.e., those associated with a “reversible” neurologic deficit and temporary loss of consciousness), it is theorized that there is temporary neurophysiologic perturbations within the reticular activating system. Although there are no grossly evident radiographic or neuropathologic lesions, neurochemical and ultrastructural changes have been observed.




Diffuse axonal injury (DAI) is the most severe form of diffuse brain injury. When the tensile strain from angular acceleration and deceleration forces act on the brain parenchyma, axons and small vessels tear. Characteristically, the head-injured patient presents with a low GCS score (3 to 8), but no gross neuroradiographic abnormalities are evident. Placement of an ICP monitor may reveal intracranial hypertension that may require intensive medical therapy over the following days (see Chapter 41). image


Unlike concussive syndromes, DAI is evident histologically throughout the callosal, periventricular, internal capsular, basal ganglia, and brain stem white matter. Tissue tear hemorrhages can occasionally be appreciated on the presenting computed tomographic scan. In fact, a grading system based on initial computed tomography (CT) results has demonstrated a correlation between computed tomographic severity of DAI and clinical outcome. When no intraparenchymal hemorrhage is present, T2-weighted magnetic resonance imaging typically demonstrates multifocal and hyperintense foci in the deep white matter structures. In postmortem studies, histologic evaluation reveals evidence of axonal injury and white matter tract disruption. Ultrastructural and immunohistochemical investigations have revealed several different mechanisms of axonal injury all culminating in irreversible disruption of the structural integrity of the axons.


Patients with DAI who remain comatose for greater than 24 hours after the initial injury tend to have a worse prognosis and, in comparison to other types of head injuries, survivors of DAI have the highest frequency of permanent neurologic disability.

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Jul 7, 2016 | Posted by in CRITICAL CARE | Comments Off on Head Trauma

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