Acute TBI Management — Vella 2017

Traumatic brain injuries can result from both blunt and penetrating mechanisms. Falls (35%) and motor vehicle collisions (17%) are the most common, with motor vehicle collisions leading to majority of fatalities. Gunshot wounds to the head are the most lethal of injuries, but, due to overall incidence, result in less total deaths. 3,4 The primary insult to the brain cannot be undone and results in brain tissue damage, impaired cerebral blood flow (CBF) regulation, and alterations in brain metabolism with upregulation of inflammatory mediators, oxidative stress, and vasospasm. These processes ultimately lead to cell death and generalized brain edema.

6 The Monro-Kellie hypothesis holds that the total intracranial volume is made up of brain tissue, cerebral spinal fluid (CSF), venous blood, and arterial blood. CBF remains constant under normal conditions via cerebral autoregulatory mechanisms over a range of blood pressures. When one compartment is increased, by a hematoma for example, there must be a compensatory decrease in another compartment in order to prevent intracranial hypertension. Cerebral perfusion pressure (CPP) is a surrogate for CBF. CPP is defined as mean arterial pressure (MAP) – intracranial pressure (ICP). A decrease in CPP implies a decrease in CBF, although this association is not perfect.

Decreased CBF ultimately leads to ischemia and hypoxia and worsening of the initial brain insult. 2,5 The goal of TBI management is to prevent this secondary insult.

Currently, we cannot reverse the initial insult causing a TBI, referred to as the primary injury. Hypotension, previously defined as systolic blood pressure <90 mmHg, and hypoxia, defined as a PaO2 ≤60 mmHg, have been associated with doubling of mortality in head injured patients.7,8 Early studies from the 1970’s showed an association between “systemic insults”, mainly hypotension, hypoxia, and hypercarbia, and increased mortality, suggesting an important role for trauma center transfer in patients with severe TBI.9 Management strategies must therefore focus on the prevention of secondary injury (i. e. hypoxia, hypotension) through maintenance of adequate CBF and prevention of hypoxia.

Consistent with all phases of TBI management, prehospital strategies should focus on preventing secondary brain injury. In one study, patients with moderate to severe TBI transferred to level I trauma centers via helicopter who had secondary insults (either SBP <90 mmHg or SpO2 <92%) were found to have a 28% mortality, compared to 20% of patients without such insults. Prehospital hypoxia in these same patients was associated with a significant increase in mortality, and there was no difference in hypoxic episodes between patients intubated vs. those not intubated in the field. 10 Similarly, prehospital rapid sequence intubation performed by paramedics in head injured patients with GCS <9 was associated with an increase in mortality.

This result may be associated with the transient hypoxia during the prehospital procedures, excessive over-ventilation causing hypocarbia, vasoconstriction, and impaired CBF, and longer scene times. 11 This body of work implies a need for rapid transfer to definitive care and a focus on more basic airway strategies to maintain

• xygenation in head injured patients.

Several studies have also evaluated the use of hypertonic saline in the prehospital arena as a means to improve CPP by decreasing ICP and increasing MAP. In a 2004 study by Cooper, et. al., patients with severe TBI (GCS <9) and hypotension (SBP <100 mmHg) were assigned to either rapid administration of 7.5% saline or a similar bolus of Ringer’s lactate by paramedics. Neurologic function at 6 months did not differ between the two groups, although mean sodium levels in the treatment group was only 149 mEq/L12 A multicenter randomized clinical trial in 2010 by Bulger, et. al. looked at patients with severe TBI (GCS <9) not in hypovolemic shock. Patients were administered either 7.5% saline/6% dextran 70, 7.5% saline alone, or 0.9% saline. Neurologic outcome at 6 months and survival did not differ among groups.13 At this time, prehospital use of hypertonic saline cannot be recommended.

The initial management of patients with TBI is identical to that of all trauma patients, focusing on the Advanced Trauma Life Support (ATLS) principles of management of airway, breathing, and circulation, followed by a rapid neurologic exam and exposure of the patient with prevention of hypothermia. 14 The airway should be secured according to local protocols. Induction agents such as propofol should be carefully used, possibly in conjunction with induction inotropes, given the risk of systemic hypotension with impaired CBF. Ketamine is an attractive agent in trauma patients given its favorable hemodynamic profile.

Despite theoretical risks, a systematic review of ketamine use in TBI suggests that ketamine does not increase ICP15 Breathing should be optimized to maintain oxygenation and prevent ventilatory dysfunction, as extremes in CO2 can lead to cerebral vasoconstriction, vasodilation, and have been shown to be predictors of morbidity and mortality. 8 Hyperventilation is used by some providers to acutely decrease ICP through hypocarbic vasoconstriction, despite evidence showing an association between even brief periods of hyperventilation and increased mediators of secondary brain injury in areas adjacent to injured brain tissue as well as local reductions in cerebral perfusion.

16–18 This strategy should be used with caution, and perhaps only employed to acutely combat signs of active herniation while initiating more definitive treatment. Circulation should be maintained to prevent hypotension and maintain CBF. There is a known coagulopathy related to head injury likely related to tissue factor release coupled with hypoperfusion, which may be exacerbated by a pure crystalloid resuscitation. A balanced blood product resuscitation has been shown to be beneficial in trauma patients,19–21 and may be extended to TBI patients. Uncrossmatched packed red blood cells are an initial resuscitative fluid choice that is often used in hypotensive trauma patients, with a goal to maintain SBP ≥90 mmHg in patients suspected of having a TBI.

The concept of permissive hypotension does not apply to patients with known or suspected TBI, and normal physiologic blood pressure parameters should be targeted in this population. During the “disability” component of the primary survey, a rapid neurologic evaluation is performed. The evaluation focuses on the pupillary exam, assesses for lateralizing signs suggesting a mass lesion with increased ICP, and calculates a GCS score to stratify the TBI severity. The patient should then be exposed to evaluate for injury and rapidly covered to prevent hypothermia. A more detailed examination is performed during the secondary survey.

Agents such as hypertonic saline and/or mannitol (discussed in more detail below) can be given during this initial resuscitation if physical exam findings suggest a neurologic decline, significant head injury, or lateralizing neurologic exam.

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