Intubation in Head Trauma

You arrive on scene of a 17 year old male pedestrian struck, unknown medical history.  A friend who was with the patient reports that they were returning from getting dinner when he was struck by a vehicle while riding his bicycle.  The friend denies any alcohol or other intoxicating substances.  The patient is combative, fighting with rescuers, and pulling at his cervical collar.  He has evidence of head trauma externally with scalp bleeding controlled with direct pressure.  You suspect that this patient has a traumatic brain injury and needs airway management to assist in his care.  You administer 4 mg midazolam intranasal to obtain mild sedation to assist with patient care.  Approximately two minutes later, the patient is more amenable to patient care efforts.  You establish IV access, place the patient on high-flow nasal cannula, and call medical control for rapid sequence intubation orders for this approximately 70 kg patient.  The physician orders 150 mcg fentanyl IVP, 100 mg ketamine IVP, and 100 mg succinylcholine IVP.  What about lidocaine?  What about defasciculating doses of a non-depolarizing paralytic?  What about the contraindication for ketamine in head trauma?

For decades, physicians and prehospital providers have been taught many myths about intubation and intracranial pressures:  Give lidocaine prior to intubation, don’t give succinylcholine without a defasciculating dose, and never give ketamine for a head injury. 

What about pretreatment for the adrenergic response to intubation?  Clinical pearl #25 addresses the use of lidocaine as pretreatment in trauma airways.  The bottom line is that some studies show that it blunts the adrenergic response to intubation and others show no significant difference.  In fact, many of the studies were actually focused on deep tracheal suctioning of already-intubated patients.  For this reason, it is not routinely recommended that lidocaine be given prior to RSI in head injury. 

If attempting to decrease intracranial pressure (ICP) and the adrenergic response to intubation (including increased HR and BP), the better medications to use are opioids, such as fentanyl 2-3 mcg/kg, or esmolol 2 mg/kg, a short-acting beta-blocker.  Fentanyl was superior to lidocaine or placebo in blunting the increase in blood pressure but not the heart rate from intubation.  In these same studies, esmolol was found to significantly blunt the increase in blood pressure and heart rate.^1–3  However, esmolol is not a typical pre-hospital medication, but it can be considered in the emergency department.  Furthermore, blunting the heart rate is typically not as critical as the blood pressure except in cases of great vessel dissection, in which the tachycardia may cause increasing shear forces on the dissection flaps.  Fentanyl also provides analgesia, which is not provided in the majority of intubations using only etomidate.

Should we be giving defasciculating doses of a non-depolarizing paralytic prior to succinylcholine?  The theory behind this stems from the mechanism of action of succinylcholine.  In order to achieve paralysis, succinylcholine activates the receptors at the neuromuscular junction, hence causing the fasciculations, and does not allow them to “reset” for the next nerve impulse.  These fasciculations are theorized to cause an increase in ICP by having many large muscle groups suddenly contracting, increasing systemic vascular resistance.  However, these fasciculations, as you know, are transient and short-lived.  In some small scale studies, succinylcholine does raise ICP in surgical patients, and a defasciculating dose does seem to block the increase.  However, this increase is transient, and the clinical significance is not known.  Furthermore, the addition of another medication for RSI results in more work for the intubating crew, especially if the non-depolarizing paralytic is vecuronium and requires dissolution in sterile water prior to drawing it up.  As a result, defasciculating doses of non-depolarizing paralytics are not routinely recommended.^4,5

Isn’t ketamine contraindicated for head trauma?  Decades ago, animal models were noted to have increased ICP when administered ketamine, and it was consequently contraindicated for years on the basis that it would decrease cerebral perfusion.  However, this is not the only variable when it comes to cerebral blood flow.  The more important number is the cerebral perfusion pressure (CPP), which is the difference between the mean arterial pressure (MAP) and the ICP à CPP = MAP – ICP.  If the MAP remains unchanged and the ICP increases, the CPP goes down, which is bad.  However, ketamine also increases MAP, and more recent studies actually show that CPP increases with ketamine.  In one study, ketamine actually decreased ICP in children.⁶  If combined with other sedatives, particularly GABA-agonists, it may also improve the post-trauma metabolism of the brain.⁷

Once again, something that has been taught for years as dogma has been based on weak, often conflicting, evidence.^8,9  Ketamine, in contrast to years of teaching, is actually an ideal induction agent for RSI in head trauma, providing analgesia and improving CPP in many instances.  However, it should be avoided in patients who are already markedly hypertensive.

References

1.                 Feng CK, Chan KH, Liu KN, Or CH, Lee TY. A comparison of lidocaine, fentanyl, and esmolol for attenuation of cardiovascular response to laryngoscopy and tracheal intubation. Acta Anaesthesiol Sin. 1996;34(2):61-7. Available at: http://www.ncbi.nlm.nih.gov/pubmed/9084524. Accessed August 31, 2014.

2.                 Gupta S, Tank P. A comparative study of efficacy of esmolol and fentanyl for pressure attenuation during laryngoscopy and endotracheal intubation. Saudi J Anaesth. 2011;5(1):2-8. doi:10.4103/1658-354X.76473.

3.                 Pouraghaei M, Moharamzadeh P, Soleimanpour H, et al. Comparison between the effects of alfentanil, fentanyl and sufentanil on hemodynamic indices during rapid sequence intubation in the emergency department. Anesthesiol pain Med. 2014;4(1):e14618. doi:10.5812/aapm.14618.

4.                 Minton MD, Grosslight K, Stirt JA, Bedford RF. Increases in intracranial pressure from succinylcholine: prevention by prior nondepolarizing blockade. Anesthesiology. 1986;65(2):165-9. Available at: http://www.ncbi.nlm.nih.gov/pubmed/2874752. Accessed August 31, 2014.

5.                 Clancy M. In patients with head injuries who undergo rapid sequence intubation using succinylcholine, does pretreatment with a competitive neuromuscular blocking agent improve outcome? A literature review. Emerg Med J. 2001;18(5):373-375. doi:10.1136/emj.18.5.373.

6.                 Bar-Joseph G, Guilburd Y, Tamir A, Guilburd JN. Effectiveness of ketamine in decreasing intracranial pressure in children with intracranial hypertension. J Neurosurg Pediatr. 2009;4(1):40-6. doi:10.3171/2009.1.PEDS08319.

7.                 Sehdev RS, Symmons DAD, Kindl K. Ketamine for rapid sequence induction in patients with head injury in the emergency department. Emerg Med Australas. 2006;18(1):37-44. doi:10.1111/j.1742-6723.2006.00802.x.

8.                 Bourgoin A, Albanèse J, Léone M, Sampol-Manos E, Viviand X, Martin C. Effects of sufentanil or ketamine administered in target-controlled infusion on the cerebral hemodynamics of severely brain-injured patients. Crit Care Med. 2005;33(5):1109-13. Available at: http://www.ncbi.nlm.nih.gov/pubmed/15891344. Accessed August 31, 2014.

9.                 Schmittner MD, Vajkoczy SL, Horn P, et al. Effects of fentanyl and S(+)-ketamine on cerebral hemodynamics, gastrointestinal motility, and need of vasopressors in patients with intracranial pathologies: a pilot study. J Neurosurg Anesthesiol. 2007;19(4):257-62. doi:10.1097/ANA.0b013e31811f3feb.