Thursday, February 14, 2013

Smoke and Mirrors: Lidocaine Pre-RSI for ICP Reduction

It's one of those things that gets hammered into the head of nearly every EM resident by their attendings during their training. That little nugget of information related to rapid sequence intubation (RSI) that is woven into the curriculum and gets passed on from class to class of EM residents who will go on to advocate it when they become EM attending physicians. We cannot help just IS. Yet, when we stare at it in the face and dig deeper into the evidence surrounding it, it is all smoke and mirrors as we realize that there really isn't much out there to substantiate the concept.

What am I referring to? The use of intravenous lidocaine as pre-medication for RSI to attenuate the increase in intracranial pressure (ICP) in patients with traumatic brain injury.

Let me start from the beginning.

The processes of endotracheal intubation and laryngoscopy can induce the cough reflex due to mechanical stimulation of the upper respiratory tract. This is compounded by the fact that these processes are associated with an increase in ICP by approximately 20 mmHg secondary to an increase in mean arterial pressure and heart rate that occurs as a result of catecholamine release. In the setting of traumatic brain injury (TBI) where ICP is already elevated, this can potentially lead to a further increase in cerebral blood volume, potentiate cerebral pefusion pressure and worsen cerebral ischemia...all of which can contribute to poor clinical outcomes.

In the 1960s, both Wycoff and Bromage were among those to have the first success with using lidocaine to blunt the cardiovascular response associated with endotracheal intubation.

Why would lidocaine work? It does suppress the cough reflex, but the mechanism by which it blunts the cardiovascular response is somewhat unclear. The thought is that as a sodium channel blocker, lidocaine may decrease cerebral metabolism and stabilize neuronal cell membranes, which may theoretically prevent secondary injury to the brain in the setting of TBI.

Here are a few studies that demonstrate the potential benefit of IV lidocaine in attenuating ICP:

An evidence-based review conducted by Robinson and Clancy aimed to determine whether patients undergoing RSI who were pretreated with IV lidocaine for acute TBI improved neurological outcomes. There was (and still is) no direct evidence that looked at the use of lidocaine in this particular setting. That is, none of the patients in these studies underwent RSI in the emergency department. The review included six studies, two of which are included in the table above, that looked at patients who received IV lidocaine that was used to attenuate the increase in ICP. These studies included patients who had monitors in place in the operating room or intensive care unit as a means to measure ICP. In addition, the studies included in this review did not aim to correlate the blunting effect of ICP associated with administration of IV lidocaine with neurological outcome or mortality.

Now let us consider the flipside: the harms associated with the use of IV lidocaine for this purpose. Lidocaine may have a dose-dependent effect in decreasing mean arterial pressure, which may potentially decrease cerebral perfusion pressure, the extent of which has not been determined. The concern for this is that if sustained for a prolonged period of time, this may lead to poor neurological outcomes. However, a recently published study did demonstrate that the use of IV lidocaine prior to RSI in patients with severe TBI was not associated with significant changes in hemodynamic status. In addition, the general recommendation for premedication in the setting of RSI is for administration to take place three minutes before intubation. From a practical point of view, this delay in time for RSI due to premedication may pose harm to the patient. In many cases, premedication may need to be foregone for immediate RSI to take place, especially in those critically ill head trauma patients.

So taking all of this into account, what is one to do? There really is no direct evidence to support the claim that IV lidocaine attenuates the increase in ICP in patients with TBI when used as a premedication for RSI. Coming to this realization should make one think twice prior to ordering it for this purpose in a patient who is going to undergo RSI. In the end, as with everything else, it really is a matter of clinical judgment.

Selected References:
Bedford RF, Winn HR, Tyson G, et al. Lidocaine prevents increased ICP after endotracheal intubation. In: Shulman K, Mamorou A, Miller JD, et al., eds. Intracranial Pressure IV. Berlin,
Germany: Springer-Verlag; 1980:595-598.
Donegan MF, Bedford RF. Intravenously administered lidocaine prevents intracranial hypertension during endotracheal suctioning. Anesthesiology 1980; 52:516-518.
Grover VK, Reddy GM, Kak VK, et al. Intracranial pressure changes with different doses of lignocaine under general anesthesia. Neurol India 1999; 47:118-121.