Month: February 2013

I made a comment once on Twitter that if I ever became a physician, the specialty I would go into would be anesthesiology. Why? Anesthesiologists have time and again done such innovative things with medications in the operating room that have made their way into the practice of emergency medicine. One example that comes to mind is the use of intravenous lipid emulsion therapy for the treatment of various toxicological emergencies. Another instance is the use of push-dose vasopressors for the short-term management of hypotension or as a bridge to vasopressor infusion therapy and/or while central line access is obtained.

In an earlier blog post, I discussed my experience with nicardipine for the management of blood pressure in the setting of neurological emergencies. Many of the studies that I have found regarding this have looked at using a continuous IV infusion of nicardipine that is titrated based on the observed blood pressure response.

So you can imagine my reaction when I discovered that the use of nicardipine as an IV bolus for the short-term management of hypertension originated from anesthesia. I thought to myself, “Those anesthesiologists have gone and done it again!” But you are probably thinking to yourself, “Wait…administration of nicardipine as an IV bolus??”

Many of the studies that have evaluated the use of bolus dosing for IV nicardipine were conducted in the perioperative setting. Bolus dosing of IV nicardipine has been used for anesthetized patients undergoing surgical procedures to control and maintain intraoperative and postoperative hemodynamic stability. Another common use of bolus dosing of IV nicardipine in the OR is for the attenuation of the increase in blood pressure associated with laryngoscopy and endotracheal intubation for patients who have undergone anesthetic induction. A great review article here highlights the results of some of these studies.

The doses that were studied in these patient populations varied between weight-based dosing (20 to 80 mcg/kg) and fixed dosing (0.25, 0.5, 1, and 2 mg). One study demonstrated a dose-dependent response associated with the use of bolus dosing of IV nicardipine and the effects on mean arterial pressure, systolic blood pressure, and diastolic blood pressure. The mean time for maximum response varied from 66 seconds to 101 seconds, depending on the dose administered.

A theoretical benefit that I can envision with the use of bolus dosing of IV nicardipine is the rapid control of blood pressure while the effects of the continuous infusion kick in. One situation where it may prove to be of some potential value is in the management of hypertension in the setting of neurological emergencies. Another setting is in the management of acute aortic dissection in patients whose blood pressure is not controlled with the use of β-blocker (i.e. esmolol) monotherapy.

Unfortunately, there have not been any trials conducted that have evaluated the use of bolus dosing of IV nicardipine in patients who are not going elective procedures, and so the applicability for patients in the emergency department is relatively limited without evidence from case studies or randomized, controlled clinical trials. Maybe one day, such studies will be performed for the acute control of blood pressure in these and other situations that are encountered in the emergency department setting. Perhaps like intravenous lipid emulsion therapy and push-dose vasopressors, bolus dosing of IV nicardipine will make its way into the practice of emergency medicine and will be heralded as one of those therapies where clinicians will wonder, “How come we never thought about using this before?” Time will tell.

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 it…it 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.