A Discussion of the Effects of Succinylcholine on Intracranial Pressure in Patients with Acute Brain Injury Requiring Rapid Sequence Intubation with or without Pretreatment with a Neuromuscular Blocking Agent- Dr. Alexander Le

Home / Respiratory / A Discussion of the Effects of Succinylcholine on Intracranial Pressure in Patients with Acute Brain Injury Requiring Rapid Sequence Intubation with or without Pretreatment with a Neuromuscular Blocking Agent- Dr. Alexander Le


Acute brain injuries (whether due to traumatic brain injury (TBI), spontaneous hemorrhage, or other cause) are a significant public health concern and major cause of morbidity and mortality worldwide. Patients with acute brain injuries frequently require mechanical ventilation, and emergent control of the airway is a time-sensitive, paramount step in management. Rapid sequence intubation (RSI) offers timely control of the airway while maintaining oxygenation and minimizing the risks of aspiration and hypercapnea. Of the choices of paralyzing agents used for RSI, succinylcholine (SCH) is widely favored due to its rapid onset and offset and consistency in achieving excellent intubating conditions.(10) In cases of acute brain injury, the use of SCH has been controversial as it has been implicated as a potential cause of increased intracranial pressure (ICP). This paper will briefly review the human evidence relating SCH to ICP, as well as the possibly mitigating practice of pretreating with a neuromuscular blocking agent prior to SCH.

A study by Minton et al is frequently cited as evidence that SCH increases ICP and a competitive neuromuscular blocker should be administered beforehand.(9) This study involved 19 patients with brain tumors undergoing elective surgery. The patients were intubated, mechanically ventilated, and anesthetized with thiopental before being given SCH alone and then SCH following a dose of vecuronium. Increases in ICP were observed with administration of SCH alone, but not when preceded by vecuronium. (The average ICP increased 4.9+2 mmHg) Of note, vecuronium was given at a full paralyzing dose (0.14 mg/kg), not the lower defasciculating dose. While this study suggests a significant rise in ICP secondary to SCH administration which is mitigated by pretreatment, it contained a small number of patients who served as their own controls and did not have acute brain injuries or undergo RSI. Furthermore, it used vecuronium at a full paralyzing dose rather than a defasciculating dose.

Another commonly cited study by Stirt et al involved 12 patients undergoing surgery for brain tumors.(11) The group of 6 patients who received SCH without pretreatment experienced increased ICPs ( Average about 10mm HG) compared to the 6 who were pretreated with metocurine 7 minutes prior to being given SCH. While this study supports pretreatment prior to SCH administration, it is small and the patients did not have acute brain injuries or undergo RSI.

A study by Marsh et al found a small, but significant increase in ICP with SCH in 8 patients having elective surgery for brain tumors.(7)

The following studies offer opposing evidence that SCH does not have a significant effect on ICP. Kovarik et al studied 10 mechanically ventilated patients with TBI in an ICU setting who were given SCH at a dose of 1 mg/kg compared to a small volume of normal saline. They did not find any significant change in ICP, mean arterial pressure, or cerebral perfusion pressure.(5)

Brown et al performed a randomized, double blind trial of 11 patients with severe TBI. The patients were intubated, mechanically ventilated, sedated and received either SCH (1 mg/kg) or normal saline of an equal volume. No significant changes in ICP or CPP were detected.(3)

White et al studied the effects of several drugs on blunting the response of ICP to endotrachial suctioning in 15 comatose ICU patients with diffuse brain injury. There was no significant change from baseline ICP after the administration of SCH and endotrachial suctioning over a fifteen minute time period.(12)

A study by Barrington et al found that administration of SCH with atropine prior to intubation prevented an increase in ICP that was found with atropine alone in 20 preterm infants, and was associated with shorter intubation times.(1)

Lam et al measured lumbar CSF pressure in 24 patients undergoing elective aneurysm clipping and did not find any significant increase in ICP after SCH administration.(6)

McLesky et al similarly looked at 4 patients undergoing elective neurosurgery for brain tumors and found no significant increase in ICP with SCH.(8)

There are unfortunately no large, randomized control trials to answer the question of the effects of SCH on ICP. The available human evidence is comprised of small studies, which demonstrate conflicting results. Similarly, there is not sufficient evidence to support the routine use of pretreatment with a neuromuscular blocking agent to blunt a possible (and questionable) increase in ICP secondary to SCH.(2,4) While the limited evidence for use of a neuromuscular blocking agent as pretreatment suggests some benefit, it should only be considered if it does not delay the establishment of a definitive airway when it is required.

1. Barrington KJ, Finer NN, et al. Succinylcholine and atropine for premedication of the newborn infant before nasotracheal intubation: a randomized, controlled trial. Crit Care Med 1989;17:1293–6.
2. BET 3: Suxamethonium (succinylcholine) for RSI and intubation in head injury
Emerg Med J 2012;29:6 511-514 doi:10.1136/emermed-2012-201374.4
3. Brown MM, Parr MJA, et al. The effect of suxamethonium on intracranial pressure and cerebral perfusion pressure in patients with severe head injuries following blunt trauma. Eur J Anaesthesiology 1996;13:474–7.
4. Clancy M, Halford S, Walls R, et al. 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, 18 (2001), pp. 373–375
5. Kovarik WD, Mayberg TS, et al. Succinylcholine does not change intracranial pressure, cerebral blood flow velocity, or the electroencephalogram in patients with neurologic injury. Anesth Analg 1994;78:p469–73.
6. Lam AM , Nicolas JF, Manninen PH. Influence of succinylcholine on lumbar cerebral spinal pressure in man. Anesth Analg1984;63:240
7. Marsh ML, Dunlop BJ, Shapiro HM, et al. Succinylcholine-intracranial pressure effects in neurosurgical patients. Anesth Analg1980;59:550
8. McLeskey CH, Cullen GF, et al. Control of cerebral perfusion pressure during induction of anesthesia in high-risk neurosurgical patients. Surv Anesthesiology 1976;20:30.
9. Minton MD, Grosslight K, et al. Increases in intracranial pressure from succinylcholine: prevention by prior nondepolarizing blockade. Anesthesiology 1986;65:165–9.
10. Perry J, Lee J, Wells G. Rocuronium versus succinylcholine for rapid sequence induction intubation. Cochrane Database Syst Rev 2003;1:CD002788.
11. Stirt JA, Grosslight KR, et al. Defasciculation with metocurine prevents succinylcholine-induced increases in intracranial pressure. Anesthesiology 1987;67:50–3.
12. White PF, Schlobohm RM, et al. A randomized study of drugs for preventing increases in intracranial pressure during endotracheal suctioning. Anesthesiology 1982;57:242–4.


  • sannman

    Bottom line: Minton’s study saying sux causes increased ICH is from 198-fricking-6, is a poor case control study, is not based on trauma, and is not done with RSI.

    Paralyzing options for intubation in head trauma:
    1) Use succinylcholine
    2) Use roc
    3) Pretreat with lidocaine 2mg/kg (not proven), then use sux
    4) Pretreat with 1/10th dose of roc (lacks good evidence), then use sux
    5) Wait for sugammadex to be approved in the US and start using roc instead of sux and reversing the roc after you finish intubating.

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