Transcript
Chapter 18: Traumatic Brain Injury
Chapter Summary
The three primary mechanisms of injury associated with traumatic brain injury (TBI) include acceleration/deceleration (most common), rotational, and penetrating. Acceleration injury occurs when the brain suddenly and rapidly moves along a linear path in one direction, and deceleration injury occurs when the brain stops moving within the cranial vault. Rotational injury occurs when the head rotates on its axis, resulting in shearing force injury to the brain and axons. Penetrating injury occurs when a foreign object (e.g., bullet, knife) invades the brain.
There are two ways in which the brain becomes injured. Primary injury results directly from the force of impact at the time of injury. Secondary injury is an indirect insult that results from the body’s response to the primary injury. Secondary injury occurs from ischemia, inflammation, neuronal death, and cerebral edema, which increases the severity of the primary injury.
There are four types of skull fractures that can result from injury to the head: linear, depressed, open, and basilar. Linear fracture is a simple fissure without fragmentation; depressed fracture has bone fragmentation that depresses down into the cranial vault; open fractures are accompanied by a scalp laceration; and basilar fractures occur at the base of the skull. All types indicate substantial force has been absorbed by the skull, and underlying brain tissue injury may be present. Open and basilar fractures carry the additional risk for infection because of exposure to outside environment. Depressed fractures can tear through the meninges and cause injury to the brain parenchyma.
TBI can result in increased intracranial volume that potentially causes intracranial hypertension, compromising cerebral perfusion and oxygenation. Three conditions can increase intracranial volume: increased brain volume, increased cerebral blood volume, or increased CSF. Increased brain volume occurs with cerebral edema or space-occupying lesions (e.g., tumor, hemorrhage, abscesses). Increased cerebral blood volume occurs with loss of autoregulation, hypoxemia, hypercapnia, or impeded venous outflow from the head. CSF volume increases when too much is produced, circulation becomes impeded, or it is not absorbed sufficiently, causing hydrocephalus. If ICP becomes too high, brain herniation occurs, as brain tissue is shifted from an area of high pressure to an area of lower pressure. Herniation is a grave complication usually leading to death.
Focal injuries occur in well-defined areas of the brain and diffuse injuries occur in several areas of the brain. Cerebral hematomas, a group of focal cerebral injuries, include epidural hematoma (EDH), subdural hematoma (SDH), subarachnoid hemorrhage (SAH), and intracranial hemorrhage (ICH).
EDH, a hematoma located between skull and dura, usually results from high-impact trauma to the temporal brain area, with rupture of the middle meningeal artery and rapidly accumulating intracranial hematoma/hemorrhage. SDH, a hematoma located between the dura and arachnoid layer, usually results from rupture of a venous vessel and slower onset of symptoms than seen in EDH. There are three types of SDH, based on the time that symptoms develop: acute, subacute, and chronic. ICH, a hematoma that develops within the brain parenchyma, can occur with trauma but is also associated with uncontrolled hypertension or ruptured aneurysm. Contusion, or bruising of the brain tissue, is another type of focal injury that can be moderate to severe in nature.
Diffuse head injury includes concussion (mild traumatic brain injury [MTBI]), diffuse axonal injury (DAI), and subarachnoid hemorrhage (SAH). MTBI, although a relatively minor injury, is associated with long-term symptoms. DAI, caused by shearing forces that disrupt neurons and cerebral blood vessels, can result in a coma that can last hours to years. The patient’s recovery from this type of injury is unpredictable. SAH, an accumulation of blood between the brain and the meningeal arachnoid layer, is usually caused by a ruptured cerebral aneurysm associated with hypertension. Patients with SAH complain of severe headache, and it may be accompanied by rapid loss of consciousness. Management of diffuse brain injuries includes therapies to reduce secondary brain injury, prevention of complications, and supportive.
A systematic neurologic assessment is performed in patients with traumatic brain injury. Determining the mechanism of injury can provide important clues regarding the type of injury that has occurred. The neurologic assessment begins directly after airway, breathing, and circulation have been stabilized. In trauma cases, the ACLS primary and secondary surveys should be performed. The Glasgow Coma Scale (GCS) is an important objective trending tool that helps grade severity of injury and evaluate changes in the patient’s neurologic status. Advanced cerebral oxygenation assessment modalities that help assess the patient’s status include brain tissue oxygen content (PbtO2) and jugular bulb oximetry (SjO2).
Management of TBI focuses on limiting the primary ischemic tissue injury and preventing/minimizing secondary injury. Cerebral perfusion pressure (CPP) is optimized through controlling the patient’s blood pressure and temperature, promoting venous return, and normalizing ICP. Intubation and mechanical ventilation is initiated if the patient’s GCS is 8 or lower to optimize PaO2 and PaCO2. Increased ICP is managed when sustained elevations of 20 mm Hg or higher occurs.
Interventions for managing TBI may include positioning techniques, controlling body temperature, placement of an intraventricular catheter for draining CSF, or possibly hyperosmolar and diuretic therapy. In severe situations, neuromuscular blockade with mild hyperventilation and mild hypothermia may be initiated. Surgical interventions may include a decompressive craniotomy, whereby a portion of the skull is removed to relieve pressure. Drugs that may be ordered to treat TBI include osmotic diuretics (mannitol), hypertonic saline, desmopressin, sedatives/hypnotics, barbiturates, and anticonvulsants.
