Traumatic Brain Injury 23.09.2020

According to the Monro-Kellie doctrine, the intracranial contents normally consist of brain tissue, intravascular blood, and CSF. If any of these components increase in volume, the others must reciprocally decrease to avoid increasing pressure. In the setting of injury, neuronal injury and death occur and lead to cytotoxic edema, which results in increased pressure and a compensatory reduction in blood flow and the production of cerebrospinal fluid. As the pressure is further elevated to high levels and cerebral perfusion continues to decrease, further neuronal death and edema occur.
The onset of edema is usually slow and reaches its maximal level within 48 to 72 hours after injury. Therefore, these patients should be monitored closely, often in an intensive care unit, over the following few days because the true neurologic sequelae of edema may not initially be obvious early after injury. The progress of cerebral edema may be monitored by neurologic examination, computed tomography, and sometimes the use of intracranial pressure–monitoring devices. These devices are commonly used to monitor patients with altered consciousness following head injury or patients with Glasgow Coma Scale scores lower than 8.
A baseline CT is initially obtained to identify intracranial hemorrhage or a mass lesion that may need to be evacuated surgically. Once these entities are ruled out, medical treatment is started to counter the progress of edema. This may be accomplished, but not necessarily in this order, by (1) elevating the head of the bed 15 to 30 degrees; (2) maintaining the patient’s head in a straight position to facilitate cerebral venous drainage; (3) temporary hyperventilation to Pco2
levels of 30 to 35 mm Hg; (4) hyperosmolar therapy and sometimes fluid restriction to minimize edema; (5) intermittent drainage of CSF through a pressure-monitoring catheter placed in the ventricular system; (6) paralytic agents to minimize patient agitation or elevated blood pressure, which may further increase ICP; and (7) neuronal burst suppressive medications to minimize cerebral metabolism and counter neuronal distress from low perfusion.
Finally, and in rare circumstances, decompressive hemicraniectomy may be indicated if enough swelling occurs from the edema and the high ICP is refractory to the aforementioned medical therapies. Frequently, the first few therapies are performed and the later, more invasive therapies are pursued only in refractory cases. Exciting experimental animal models using neuroprotective agents have not shown the same beneficial effects in humans when translated to clinical trials. New research on induced hypothermia has demonstrated promise in small case studies, but larger randomized trials have not yet been performed.
Steroids are believed to decrease vasogenic edema by limiting the permeability of the vasculature, but they have not been shown to impede cell death from trauma or limit cytotoxic edema. No meta-analysis has been performed, but the largest trial to date on traumatic brain injury demonstrated an increase in mortality with steroids, and therefore steroids are not recommended.

Cerebral perfusion pressure is calculated by the formula CPP = MAP − ICP, where MAP is mean arterial pressure. Therefore, as intracranial pressure rises to malignant levels, CPP falls. This is problematic in the treatment of elevated ICP, because attempts to continue perfusing the brain (elevating CPP) can occur only by elevating blood pressure (MAP). Increasing blood pressure with already elevated ICP leads to loss of the brain’s normal autoregulatory mechanisms, which eventually results in even higher ICP. Much debate exists over whether to focus treatment on CPP or ICP. Early studies indicated that greater than a 20-mm Hg elevation in ICP for sustained intervals was associated with poor neurologic outcome. Later studies indicated that CPP less than 60 mm Hg was also associated with worse outcome. Recent preliminary studies, however, have shown that aggressive maintenance of CPP at a level higher than 60 mm Hg, even with prolonged ICP higher than 50 mm Hg for more than 48 hours, may still lead to a good neurologic outcome. Further randomized trials need to be performed before definitive recommendations can be made. Unfortunately, there are no level I studies indicating an optimal CPP threshold or ICP limit on which to base CPP-guided therapy.
The initial steps in controlling elevated ICP include medical therapies such as raising the head of the bed, maintaining the patient’s head straight, hyperventilation, and hyperosmolar therapy. Hyperventilation is a quick and easy way to lower ICP in theory, for lowering Pco2 will decrease cerebral blood flow and reverse brain parenchymal and CSF acidosis. However, hyperventilation is not without consequence. Disadvantages include induced vasoconstriction to a point where ischemia develops. The alkalization of cerebrospinal fluid is also very short-lived with hyperventilation. In a direct comparison of hyperventilation and no hyperventilation in patients with severe head injury, some studies have shown a statistically significant worse outcome in the hyperventilation group, mainly because of ischemia induced by the prolonged therapy. However, temporary hyperventilation is still a useful tool to lower ICP until other measures can be instituted.
The usual hyperosmolar agents used in the setting of traumatic brain injury are mannitol and hypertonic saline. Mannitol has three postulated effects: (1) plasma expansion, which improves cerebral rheology; (2) antioxidant effect, which improves the cerebral reaction to ischemia; and (3) osmotic diuresis, which lowers MAP and then ICP in a slightly delayed fashion. This third mechanism, however, could be detrimental if diuresis decreases MAP to a point of reduced CPP. Regardless, a level III randomized controlled trial has shown improved outcome with mannitol therapy. Hypertonic saline, in contrast, reduces ICP while preserving or improving CPP. Although it is questioned whether the reduction in ICP by hypertonic saline is greater than that by mannitol, few studies have directly compared the two, and they are rarely compared in equimolar doses. Additionally, despite hypertonic saline’s proved effect on control of ICP, no evidence of improved outcome exists. As a result, there is insufficient evidence to support the use of hypertonic saline over mannitol for osmotherapy in adults. Hemicraniectomy has an important role in the treatment of elevated ICP; however, it is rarely used as first-line therapy except in some cases of malignant stroke.

Initial care of a head-injured patient must focus on maintenance of ventilation, control of hemorrhage, and maintenance of the peripheral circulation as in any trauma scenario. Continued hypotension and tachycardia are rarely the direct results of head trauma and should alert the examiner to the existence of a
systemic hemorrhage. Normal intracranial volume is only 1300 cm3 in adult females and 1500 cm3
in adult males, which makes severe blood loss intracranially nearly impossible.
Instead, severe intracranial trauma more commonly leads to the Cushing triad (hypertension, bradycardia, and irregular respirations).
As soon as possible, careful neurologic examination and documentation of the level of consciousness should be undertaken as a baseline for later comparison as the patient progresses.
Decerebrate posturing (extension and internal rotation of the extremities, neck extension, and arching of the back) implies compression of or damage to the brainstem below the level of the red nucleus (midbrain).
The Glasgow Coma Scale measures motor, verbal, and eye responses on scales of 1 to 6, 1 to 5, and 1 to 4, respectively. It is recorded as a sum of the highest score in each category, and the lowest possible total score is 3. Coma is defined by a GCS score of 8 or less. Patients with a score lower than 5 have a mortality rate higher than 50%. Scores of 3 are associated with mortality approaching 100%.
The syndrome of inappropriate antidiuretic hormone secretion should be suspected when serum osmolality and sodium levels fall in association with an increase in urinary osmolality. Restriction of water intake or the use of solute diuretics may be necessary to control this problem. SIADH sometimes needs to be differentiated from cerebral salt wasting (CSW), in which brain trauma induces the active secretion of sodium. Although the resultant hyponatremia and low serum osmolality are similar to SIADH, treatment of CSW focuses more on serum sodium replacement with hypertonic saline as opposed to fluid restriction.

The overall incidence of traumatic cerebrospinal fluid leak is 0.25% to 0.50%. It occurs secondary to a skull fracture that tears the dura. If a CSF leak is suspected, the fluid may be sent for determination of β2
-transferrin because this protein only exists in CSF and the vitreous of the eye. Imaging studies may then be useful in identifying the site of leakage after one is suspected.
Most traumatic cerebrospinal fluid fistulas close spontaneously within a few days, but they may be managed in the hospital under close supervision. Placement of a lumbar drain to divert the fistula can be helpful if spontaneous resolution does not occur.
The risk for persistent drainage and infection is greater with rhinorrhea than with otorrhea. If left untreated, both rhinorrhea and otorrhea may eventually lead to infection, but some patients can go for years without sequelae. Initial treatment involves bed rest, elevation of the head of the bed, and stool softeners to prevent straining.
The use of prophylactic antibiotics remains a controversial issue. Proponents believe that CSF leaks are exposed to upper respiratory tract and skin pathogens and are therefore at high risk for infection. Opponents argue that despite the exposure, prophylactic antibiotics contribute to antibiotic resistance and, moreover, that prophylactic antibiotics do not decrease the risk for meningitis. The evidence available does not support the use of prophylactic antibiotics, whether a skull fracture exists in isolation or with a CSF leak. However, if meningitis is confirmed, antibiotic therapy is started based on sensitivity of the organism. Surgical exploration may be indicated for leaks refractory to observation and lumbar drainage to repair the torn dura if the site of CSF leak can be found.

Neurogenic shock should be suspected in any patient with cervical spinal cord trauma. It is characterized by the sudden loss of sympathetic tone and the predominance of parasympathetic tone. Sympathetic control starts in the hypothalamus and is carried down the brainstem through the spinal cord, where it exits to target organs at the thoracic and high lumbar levels. Therefore, any damage to the cervical cord may disrupt descending sympathetic neurons. Common features of neurogenic shock include hypotension, bradycardia, warm and dry extremities, peripheral vasodilation, venous pooling with decreased cardiac output, poikilothermia, and priapism. In contrast to other forms of shock, loss of sympathetic tone in patients with neurogenic shock leads to both hypotension and bradycardia. As smooth muscle in the vasculature relaxes and blood pressure decreases, cardiac drive is also lost and reflexive tachycardia cannot be accomplished. Firstline therapy is similar to that for other forms of shock and may involve placing the patient in the Trendelenburg position, fluid resuscitation, or administration of vasopressor agents, but a few key points differ. Because of loss of vasomotor tone, massive fluid boluses with crystalloids may result in flash pulmonary edema. Pressor agents are often useful, but an agent with only α-adrenergic properties may lead to unopposed reflexive bradycardia, which may worsen cardiovascular dynamics. An agent such as dopamine with both α- and β-adrenergic properties will combat any reflexive bradycardia and is the preferred medication. In any trauma with suspected cervical injury, a cervical collar is recommended until the spine is cleared. However, the pure absence of a cervical collar should never be used to rule out either cervical trauma or neurogenic shock.