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Trauma to the Brain
Traumatic brain injury (TBI) is a worldwide major source of lifelong morbidity and mortality. It is the leading cause of death in North America for individuals between the ages of 1 and 45. The societal cost is substantial, with approximately 2.5 million emergency department visits per year and 3–5 million Americans living with a TBI-related disability. Many of these injuries involve young individuals; contact sports and motor vehicle accidents are the most common causes of TBI in individuals 15–19 years old. Of patients with severe TBI, about 40% die from their illness and 60% will have lifelong disability. Young men are overrepresented in this illness. Individuals over 75 have the highest rates of hospitalization and death among all age groups with TBI. Coexisting medical conditions and higher rates of anticoagulation contribute to the increased severity in this population.
Various head injury classification systems exist. These are based on (1) severity (mild, moderate, severe), (2) mechanism (closed vs. penetrating), (3) skull fractures (depressed vs. nondepressed), (4) presence of intracranial lesions (focal vs. diffuse), and (5) hemorrhages (extraaxillary epidural or subdural, subarachnoid, focal parenchymal/lobar, or brainstem Duret hemorrhage).
TBI is a sequence of two related processes: primary and secondary brain injury. Primary brain injury is a result of the initial event such as direct impact, penetrating injury, acceleration/deceleration injuries, and others. Secondary brain injury occurs as a result of a sequence of multiple cascades of molecular injuries that results in cell death and brain swelling.
Clinical Vignette
An emergency physician is requesting an emergent evaluation for a 26-year-old male who was transferred to your emergency room by ambulance after being hit by a speeding car. Eyewitnesses report that the patient lost consciousness for less than a minute after the accident but he then regains consciousness and is able to ambulate afterward. En route to the emergency room his mental status declines. On physical examination upon admission to the emergency room, his Glasgow Coma Scale (GCS) is 5. His right pupil is 11 mm and nonreactive. After emergency endotracheal intubation and application of a cervical collar application, computed tomography (CT) of the head is performed in addition to body imaging, and shows a lens-shaped density compressing the right parietal lobe and a small fracture of the right temporal bone consistent with an epidural hematoma. Body imaging shows multiple fractured ribs on the right side and a tension pneumothorax. A right-sided chest tube is emergently placed and the patient is emergently transferred to the operating room where he has a craniotomy and evacuation of the hematoma.
Comment: This patient presents with a classic history of epidural hematoma (EH). He has an initial lucid interval but soon after his mental status deteriorates as the hematoma size expands and compresses his brain, resulting in transtentorial herniation.
General Principles of Head Injury Care
The initial management of severe head injuries follows the Advanced Trauma Life Support guidelines by the American College of Surgeons. Most often, patients have other injuries warranting resuscitation and a primary and secondary trauma survey, which consists of:
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A— Airway: Assess airway patency and establish a patent airway and cervical immobilization with neck collar.
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B— Breathing: Evaluate rate, rhythm, and breath sounds. Provide ventilatory support if indicated.
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C— Circulation: Assess for external source of bleeding, heart rate, skin color, and blood pressure.
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D— Disability — Neurologic: Assess level of consciousness using Glasgow Coma Scale ( Fig. 19.1 ), evaluate pupil size and reaction, assess for lateralizing neurologic signs or spinal cord injury.
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E— Exposure/Environmental Control: Expose the patient for comprehensive assessment and prevent hypothermia.
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Secondary Survey & Management: This includes head-to-toe evaluation and examination to assess for possible injuries and provide initial management.
Concomitantly, the patient's general level of responsiveness must be assessed using the GCS ( Fig. 19.1 ). The lowest possible score of 3 means that individuals have no ability to open their eyes, no motor response to verbal command or direct stimuli, and no verbal response to the physician's questions, giving a score of 1 for each of the three components. The highest possible score is 15 in a fully alert and responsive individual. A complete examination of the exterior surface of the face and head is vital. Blood loss can be extensive given the location of blood vessels within the dense connective tissue of the scalp, which decreases retraction of cut vessels and promotes bleeding.
Skull Fractures
Skull fractures can be located in the calvarium (vault) and/or the basal skull. Fractures of the cranial vault carry a 20 times greater incidence of intracranial hematoma in comatose patients and a 400 times greater incidence in conscious patients. Basal skull fractures, often difficult to identify on head CT, can present with pathognomonic signs, including raccoon or panda bear eyes, battle sign (ecchymosis over the mastoid process), and cerebrospinal fluid (CSF) leakage from the nose, throat, or ears ( Fig. 19.2 ). Most leaks resolve spontaneously. Persistent leaks necessitate operative treatment ( Fig. 19.3 ).
Depressed fractures and those along the temporal bone are more commonly associated with injury to the brain or blood vessels. A fracture across the middle meningeal artery may produce an epidural hematoma (EH). Open fractures with their communication between the intracranial vault and the external environment are associated with higher risks of spinal fluid leaks and infection ( Fig. 19.4 ).
Extraaxial Traumatic Brain Injuries
Traumatic Subarachnoid Hemorrhage
Subarachnoid hemorrhage (SAH) is the most common sequela of TBI and is typically associated with additional intracranial lesions. SAH can range from clinically asymptomatic to fatal. These SAH blood products can obstruct CSF circulation or reabsorption, leading to increased intracranial pressure (ICP) with hydrocephalus. Depending on the severity of the hemorrhage, treatment of traumatic SAH may include placement of a ventricular drain or shunting system for secondary hydrocephalus.
Epidural Hematomas
EH represents an acute blood collection contained between the dura and inner table of the skull. These occur in approximately 2% of all TBIs ( Fig. 19.5 ) and 5%–15% of fatal head injuries. EHs most commonly develop in the temporal and parietal regions; 90% of EH are associated with a skull fracture that results in lacerations of vascular structures, more commonly the middle meningeal artery ( Fig. 19.6 ) or, less commonly, venous injuries.
Immediately after the closed head injury, the patient classically experiences an initial but relatively brief loss of consciousness secondary to the primary concussive injury. This is then followed by a “lucid interval” with return of wakefulness, which can be reassuring. Subsequently, as the torn vessels leak and the EH expands, regional brain compression leads to a rapid lapse into coma (see Fig. 19.3 ). This presentation occurs in less than one-third of affected individuals. Most patients do not have a lucid interval. Cranial CT imaging usually demonstrates a hyperdense, biconvex collection between the skull and brain ( Fig. 19.7 ). EHs do not cross cranial suture lines and they expand in thickness under the effect of high pressure arterial bleeding. On occasion, the initial CT is normal. Thus, when the patient is at high risk (i.e., moderate to severe TBI and/or skull fractures) it is essential to closely observe the patient's neurologic exam and level of consciousness and to repeat the CT scan at the slightest clinical change. Once the EH is identified, emergency surgical evacuation is indicated. EHs are one of the most serious sequelae of brain trauma and can be fatal without immediate recognition and surgical evacuation.
Clinical Vignette
An 85-year-old man is being evaluated in the Emergency Department (ED) for weakness. He reports headache, dizziness, and weak legs for the past few days. On further questioning, he recalls that 7 weeks earlier he had slipped on the ice, striking his occiput, while helping to push a car out of a snow bank.
His neurologic examination is significant only for tandem ataxia but is otherwise unremarkable. Head CT demonstrates large biparietal subdural hematomas. Bilateral craniotomies are performed, draining both hematomas. Postoperatively, he has a few focal motor and sensory seizures that stopped after he was started on phenytoin. His neurologic and functional recovery is otherwise excellent.
Acute Subdural Hematoma
Subdural hematomas (SDHs) are located between the arachnoid and the dural membranes and are classified by their temporal profile. Acute SDHs occur in 15% of TBI patients; these are seven to eight times more common than EHs. Advanced age is associated with greater risk because of atrophy of the cerebral cortex. With cerebral atrophy, an increasing space develops within the subdural compartment. In turn this leads to increased stretch on the bridging veins between the skull and the surface of the brain ( Fig. 19.8 ). When any individual sustains direct head trauma, the brain parenchyma accelerates and decelerates in relation to fixed dural structures. This leads to a tearing of the now anatomically stretched veins that form a “bridge” between the cerebral cortex and the skull. Concomitant injury to cortical arteries can also lead to bleeding into the subdural space ( Fig. 19.9 ).
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