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Airway management in the patient with elevated ICP for emergency medicine and critical care

Airway management in the patient with elevated ICP for emergency medicine and critical care
Authors:
Andy Jagoda, MD
Cappi Lay, MD
Section Editor:
Ron M Walls, MD, FRCPC, FAAEM
Deputy Editor:
Michael Ganetsky, MD
Literature review current through: Jan 2024.
This topic last updated: Sep 19, 2022.

INTRODUCTION — Patients with acute elevations in intracranial pressure (ICP) from trauma, stroke, infection of the central nervous system, or other processes often require emergency airway management. In managing these patients, certain medications and techniques reduce the likelihood of major fluctuations in cerebral perfusion pressure, which can exacerbate brain injury.

This topic will discuss emergency airway management in patients with elevated ICP outside the operating room. Other aspects of emergency airway management and diseases that cause elevations in ICP are reviewed separately.

●For further discussion of emergency airway management: (see "Basic airway management in adults" and "Overview of advanced airway management in adults for emergency medicine and critical care" and "Rapid sequence intubation in adults for emergency medicine and critical care" and "Rapid sequence intubation (RSI) in children for emergency medicine: Approach").

●For discussions of injuries and diseases that elevate ICP: (see "Evaluation and management of elevated intracranial pressure in adults" and "Skull fractures in adults" and "Management of acute moderate and severe traumatic brain injury" and "Overview of the evaluation of stroke" and "Management of vasogenic edema in patients with primary and metastatic brain tumors" and "Severe traumatic brain injury (TBI) in children: Initial evaluation and management").

PATHOPHYSIOLOGY — Cerebral perfusion pressure (CPP) is the driving force for blood flow to the brain. It is calculated by taking the difference between the mean arterial blood pressure (MAP) and the intracranial pressure (ICP), as expressed in the formula CPP = MAP – ICP. The pathophysiology of elevated ICP is discussed in detail separately; issues of particular relevance to airway management are highlighted below. (See "Evaluation and management of elevated intracranial pressure in adults" and "Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis".)

Autoregulation is the ability to regulate cerebral blood flow (CBF) over a wide range of MAPs. CPP is typically preserved through a MAP range of approximately 60 to 160 mmHg. When severe intracranial hypertension develops, autoregulation often is impaired. In this setting, excessive systemic hypotension can aggravate brain injury by causing cerebral hypoperfusion and hypoxemia, with resultant cerebral edema and increasing ICP. Hypotension is especially harmful and must be anticipated and avoided whenever possible. Mild permissive systemic hypertension might be necessary in the setting of increased ICP to maintain cerebral perfusion. Excessive hypertension, especially in the setting of impaired autoregulation, can further increase ICP.

Patients with intracranial hypertension present a particular clinical challenge, since many airway management techniques potentially increase ICP. Often, these patients are the victims of multiple trauma and present with hypovolemia with or without hypotension, thus limiting the choice of agents and techniques available.

In such cases, it might appear that increases in MAP would be beneficial by allowing CPP and oxygenation of brain tissue to be maintained. However, because of the loss of autoregulation in patients with intracranial injury, increases in MAP can translate directly into increases in ICP. Thus, not only is the driving gradient for CPP increased, but the absolute ICP is increased as well. Accordingly, it is important to try to maintain the MAP in a reasonable range (approximately 100 to 110 mmHg) to optimize cerebral perfusion and to minimize absolute ICP.

The techniques and medications used in airway management may increase ICP through several mechanisms. These include the reflex sympathetic response to laryngoscopy (RSRL), other reflexive responses to stimulation and manipulation of the upper airway (eg, laryngoscopy and placement of the endotracheal tube), and the direct increase in ICP stimulated by certain medications used during intubation [1,2]. Likewise, medications used in rapid sequence intubation (RSI) may cause sympatholysis with consequent hypotension; thus, having phenylephrine available at the bedside may be helpful.

The RSRL is stimulated by the sensory innervation of the supraglottic larynx, which results in increased serum levels of epinephrine, norepinephrine, and vasopressin [3-5]. The innervation of the upper and lower airways is discussed in detail separately. (See "Neuronal control of the airways".)

Use of the laryngoscope or attempted placement of an endotracheal tube results in a significant afferent discharge that increases cardiovascular sympathetic activity. For direct laryngoscopy attempts up to 45 seconds in duration, the longer the attempt the greater the sympathetic nervous system stimulation [6]. Both the lighted stylet and fiberoptic techniques result in reflex sympathetic responses that are comparable to direct laryngoscopy [4,7-9].

The catecholamine surge caused by RSRL leads to an increased heart rate and blood pressure, which significantly enhances cerebral blood flow (CBF) through redistribution and increased cerebral blood volume [10,11]. Ultimately, these hemodynamic changes can exacerbate intracranial hypertension if autoregulation is impaired, and therefore, it is desirable to mitigate such responses.

RAPID SEQUENCE INTUBATION FOR ELEVATED ICP — We believe rapid sequence intubation (RSI) is the preferred method for securing the airway in patients with suspected elevated intracranial pressure (ICP). This recommendation is based upon its high success rate and low incidence of complications. However, no outcome studies have been performed to determine the best approach to airway management in these patients.

RSI protocols are designed to minimize potentially adverse reactions, such as the reflex sympathetic response that occurs during airway manipulation. Assessment of the airway and the performance of RSI are discussed separately. (See "Approach to the difficult airway in adults for emergency medicine and critical care" and "Rapid sequence intubation in adults for emergency medicine and critical care" and "Rapid sequence intubation (RSI) in children for emergency medicine: Approach".)

When performing RSI in the patient with elevated ICP, gentle, controlled technique is desired and prolonged or multiple attempts at intubation should be avoided whenever possible. Minimizing stimulation of the supraglottic larynx reduces the reflexive responses that can exacerbate elevations in ICP. (See 'Pathophysiology' above.)

The use of RSI in patients with the potential for neurologic deficits carries the responsibility of performing and documenting an appropriate neurologic evaluation, when possible, prior to the initiation of neuromuscular blockade. The assessment should include the patient's ability to interact with surroundings, pupillary reflexes, and motor response to voice and pain. The careful recording of these findings establishes a baseline for comparison during subsequent monitoring, as well as providing important prognostic information.

Maintaining oxygenation is vital in patients with elevated ICP. Preoxygenation plays an important role in RSI by allowing the clinician to maintain high oxyhemoglobin saturation without requiring bag-mask ventilation while neuromuscular blockade takes effect, thereby minimizing the risk of aspiration. However, if the patient's oxygenation is compromised, positive pressure ventilation with a bag and mask may be required throughout the pre-intubation sequence. In such circumstances, the increased risk of aspiration is offset by the hazard of inadequate oxygenation. (See "Rapid sequence intubation in adults for emergency medicine and critical care", section on 'Preoxygenation'.)

Do not forego appropriate induction and neuromuscular blocking agents in the comatose patient who is to undergo RSI. The pathologic reflexes described above do occur in comatose patients, though they may appear unresponsive [12].

PRETREATMENT AGENTS FOR RSI

Overview and approach — Intracranial pressure (ICP) can increase as a result of the reflex sympathetic response to laryngoscopy (RSRL) and direct reflexive responses to airway manipulation. The mechanisms by which these responses occur are outlined above. (See 'Pathophysiology' above.)

In a patient whose condition would be exacerbated by a rise in ICP, when time allows, we suggest pretreatment with a short-acting opioid (eg, fentanyl) to blunt the rise in ICP caused by the adverse responses during rapid sequence intubation (RSI) discussed above. Such conditions may include acute brain injury, ischemic stroke, intracranial hemorrhage, meningitis or encephalitis, cerebral edema, and hypertensive encephalopathy (table 1). (See "Evaluation and management of elevated intracranial pressure in adults".)

We give fentanyl 3 mcg/kg intravenously (IV) over 30 to 60 seconds. Fentanyl should not be given to hypotensive patients or patients with hypovolemia who are dependent upon sympathetic drive to maintain a minimally compensated blood pressure.

No outcome studies have demonstrated that transient increases in ICP result in worse patient outcomes, and the use of pretreatment medications should be viewed as supplementary (ie, nonessential) in RSI. Nevertheless, short-acting opioids are relatively safe and may be beneficial when given in the proper setting. (See 'Ultra-short acting opioid' below.)

The findings of studies of the effects of lidocaine on elevated ICP are inconsistent and we no longer suggest pretreatment with lidocaine. While short-acting beta blockers (ie, esmolol) minimize reflex hypertension and tachycardia due to laryngoscopy, they are not used in the acute trauma setting because of the risk of hypotension. The use of a defasciculating dose of a nondepolarizing neuromuscular blocking agent to reduce the ICP response that occurs during the fasciculations caused by succinylcholine is of unproven benefit and is not recommended. (See 'Lidocaine' below and 'Beta blocker' below and 'Defasciculating dose of NMBA' below.)

Ultra-short acting opioid — A single pretreatment dose of an ultra-short acting opioid (eg, fentanyl, alfentanil, sufentanil) given over 30 to 60 seconds mitigates the RSRL without causing hypoventilation or respiratory depression.

Multiple small randomized trials have demonstrated the effectiveness of fentanyl in this regard when given at a dose of 5 mcg/kg IV [13-15]. However, this dose may cause premature respiratory depression during RSI. Some observational trials found that fentanyl, at a dose of 2 to 3 mcg/kg IV, mitigates the RSRL [16], but other studies found no benefit unless esmolol was given concurrently [17-19]. Administering a reduced dose of fentanyl (3 mcg/kg) seems to provide the best balance between the desired (sympathetic blockade) and undesired (respiratory depression) effects.

Alfentanil showed superior hemodynamic attenuation of RSRL in one study, but is relatively unknown to emergency physicians and not used for other purposes in emergency practice [20].

Lidocaine — There is no high quality evidence that directly addresses whether pretreatment with lidocaine effectively reduces the rise in ICP caused by laryngoscopy and endotracheal intubation (ETI) [21,22]. In small, randomized and nonrandomized clinical trials, IV lidocaine has shown mixed and inconsistent attenuation of the blood pressure and pulse response to ETI [11,16,23-25]. Studies of the drug's effect upon ICP also report inconsistent results. Several small randomized trials have found that lidocaine minimizes the rise in ICP in patients undergoing neurosurgical procedures [26] or endotracheal suctioning [27-29]. In contrast, other randomized trials have found no benefit from pretreatment with lidocaine in blunting ICP rise during ETI [30] or endotracheal suctioning [31].

Given these conflicting studies, we believe there is insufficient evidence to recommend that lidocaine be used as a pretreatment agent for patients with elevated ICP undergoing RSI.

Beta blocker — In multiple small randomized trials, the short-acting beta blocker esmolol, given at a dose of 2 mg/kg IV, has demonstrated the ability to control both heart rate and blood pressure responses to intubation [17,32-34]. Unfortunately, esmolol may cause hypotension, which must be avoided at all costs in the head-injured patient. For this reason, although esmolol is consistent and reliable for mitigation of RSRL in elective anesthesia, it is generally not used for this purpose in the emergency department.

Defasciculating dose of NMBA — There is no high quality evidence to support the use of a small (ie, defasciculating) dose of a nondepolarizing neuromuscular blocking agent (NMBA) to blunt the potential rise in ICP caused by the fasciculations that accompany succinylcholine (SCh) administration [35]. This practice adds complexity to airway management without clear benefit and we do not suggest such treatment.

CHOICE OF INDUCTION AGENT FOR RSI — We suggest that etomidate (0.3 mg/kg intravenous [IV] push) be used as the induction agent for rapid sequence intubation (RSI) in patients with elevated ICP, particularly those who are hypotensive or at risk for hypotension. Ketamine (1 to 2 mg/kg IV) can also be used as the induction agent in normotensive or hypotensive patients. For patients with elevated ICP who are at no risk of hypotension, sodium thiopental may be used. Induction agents for RSI are discussed in detail separately; some aspects relevant to their use in patients with elevated ICP are described here. (See "Induction agents for rapid sequence intubation in adults for emergency medicine and critical care".)

Etomidate is a short-acting imidazole derivative with rapid onset, stable hemodynamics, and minimal impact on respiratory drive. Etomidate has a safe hemodynamic profile, even when used in patients who are hypovolemic or cardiovascularly impaired. It has been shown to decrease the basal metabolic rate of oxygen utilization of the brain (CMRO2) and ICP in a fashion similar to thiopental [36,37].

Ketamine is a dissociative anesthetic with analgesic and amnestic properties. Among its many effects, ketamine stimulates catecholamine receptors leading to increases in mean arterial blood pressure and cerebral blood flow. Thus, we believe ketamine is an appropriate induction agent for normotensive or hypotensive patients with elevated ICP. However, the use of ketamine in head-injured patients remains controversial among some clinicians; this issue is discussed separately. (See "Induction agents for rapid sequence intubation in adults for emergency medicine and critical care", section on 'Ketamine'.)

Methohexital is a short-acting barbiturate that provides a cerebroprotective effect by decreasing CMRO2. In addition, methohexital decreases cerebral blood flow, thus decreasing ICP. This ability to decrease both ICP and CMRO2 makes methohexital attractive. However, methohexital is a negative inotrope and vasodilator that can ultimately reduce mean arterial blood pressure and CPP [38]. Consequently, methohexital should only be used in patients with stable hemodynamics, and even then should be used with caution.

CHOICE OF NEUROMUSCULAR BLOCKING AGENT FOR RSI — We suggest that succinylcholine (SCh; 1.5 mg/kg intravenously [IV]) be used as the neuromuscular blocking agent (NMBA) for rapid sequence intubation (RSI) in patients with elevated ICP because of its rapid onset, consistent and reliable effects, and short duration of action [39]. NMBAs for RSI are discussed in detail separately; their use in patients with elevated ICP is described here. (See "Neuromuscular blocking agents (NMBAs) for rapid sequence intubation in adults for emergency medicine and critical care".)

In animal studies, SCh causes a temporary increase in intracranial pressure (ICP) during the fasciculation phase [40,41]. However, one small observational study in humans showed no such effect [42], and the clinical significance of this phenomenon remains unknown.

The administration of a small "defasciculating" dose of a nondepolarizing NMBA or a mini-dose (20 mg) of succinylcholine has been used to reduce fasciculations, but the effect of these practices upon ICP remains unclear and this approach is no longer recommended. (See 'Defasciculating dose of NMBA' above.)

Contraindications to the use of SCh include the following:

●Malignant hyperthermia history (personal or family)

●Neuromuscular disease involving denervation (note SCh is safe in myasthenia gravis)

●Muscular dystrophy

●Stroke over 72 hours old

●Rhabdomyolysis

●Burn over 72 hours old

●Significant hyperkalemia (eg, suggested by characteristic changes on an electrocardiogram)

Nondepolarizing (ie, competitive) NMBAs do not cause an elevation of ICP. Rocuronium is the most commonly available short-acting competitive agent. However, although rocuronium is relatively short-acting, spontaneous respiration does not return for up to 45 minutes after its use if a reversal agent (ie, sugammadex) is not given. Studies have not demonstrated an outcome benefit to the use of a nondepolarizing versus a depolarizing NMBA. Some clinicians use "double-dose" rocuronium to mimic the effects of succinylcholine without its potential downsides, but this approach can delay performing an accurate neurologic examination for up to two hours, and this risk must be carefully weighed against any potential benefit.

AWAKE INTUBATION — Rarely, an "awake" approach to intubation may be preferable when a difficult airway is predicted in patients with elevated ICP. Awake intubation is discussed further separately. (See "Induction agents for rapid sequence intubation in adults for emergency medicine and critical care", section on 'Conditions precluding use of a paralytic'.)

The risks and benefits of awake intubation must be weighed carefully in this setting due to the risk of further elevations in ICP from the stimulatory effects of intubation. The most gentle intubation technique possible, usually flexible fiberoptic intubation, should be used.

Although patients with elevated ICP have a decreased level of consciousness, the use of topical anesthesia, intravenous (IV) sedation, and IV opioid analgesia is advisable. When time permits, a drying agent (eg, glycopyrrolate 0.2 to 0.4 mg IV) improves the efficacy of topical anesthetics and should be used. Topical anesthesia, such as lidocaine 4%, can be combined with a vasoconstrictor, such as topical phenylephrine 0.5%, and administered via nebulizer [43]. The choices of sedative agent and opioid analgesic are the same as for the patient with normal intracranial pressure and are guided by assessment of the patient's hemodynamic and respiratory status.

INITIATING MECHANICAL VENTILATION — Mechanical ventilation in the patient with elevated intracranial pressure (ICP) should be predicated upon three principles:

●Optimize oxygenation

●Prevent hypocapnia

●Avoid ventilation mechanics that increase cerebral venous congestion (eg, positive end-expiratory pressure, high peak inspiratory pressure)

Reduction in PaCO2 tensions in the brain leads to vasoconstriction, decreased cerebral blood flow, and decreased ICP. Therefore, patients should be ventilated in such a way as to target the lower limits of normocapnia (PaCO2 of 35 mmHg). Hypocapnia (PaCO2 <35) is linked to worse patient outcomes in both prehospital [44] and in-hospital studies [45]. Consequently, carbon dioxide tension should be followed with continuous capnography and correlated with arterial blood gas analysis. Hyperventilation to a PaCO2 of 30 mmHg should only be used when osmotic agents and CSF drainage are not effective in managing an acute rise in ICP that is accompanied by neurologic deterioration.

Long-term analgesia and sedation should be used as needed to permit effective mechanical ventilation, minimize sympathetic response, and reduce elevated ICP. Postintubation sedation is best accomplished with propofol or midazolam, which reduce the cerebral metabolic rate of oxygen (CMRO2) and contribute to lowering ICP. Opioids do not lower the CMRO2 and have an unpredictable effect on ICP, and thus we recommend that they be avoided if possible. If these measures are ineffective, pharmacological paralysis may be needed. Further discussion of mechanical ventilation and monitoring in the setting of elevated ICP is found separately. (See "Mechanical ventilation of adults in the emergency department", section on 'Elevated intracranial pressure' and "Evaluation and management of elevated intracranial pressure in adults" and "Mechanical ventilation of adults in the emergency department", section on 'General IPPV'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Airway management in adults".)

SUMMARY AND RECOMMENDATIONS

●Airway management and increased intracranial pressure (ICP) – The techniques and medications used in airway management may increase ICP through several mechanisms. Such elevations can cause harm in patients whose ICP is already high due to acute brain injury, ischemic stroke, intracranial hemorrhage, meningitis or encephalitis, cerebral edema, and hypertensive encephalopathy. (See 'Pathophysiology' above.)

●Rapid sequence intubation (RSI) – RSI is the primary method for securing the airway in patients with suspected elevated ICP whose airways are not anticipated to be difficult. Assessment of the airway and the performance of RSI are discussed separately. (See "Approach to the difficult airway in adults for emergency medicine and critical care" and "Rapid sequence intubation in adults for emergency medicine and critical care" and "Rapid sequence intubation (RSI) in children for emergency medicine: Approach".)

●Pretreatment with fentanyl – Pretreatment medications are optional when performing RSI. When time allows, we suggest pretreatment with a short-acting opioid (eg, fentanyl) to blunt the rise in ICP during RSI in patients whose condition would be exacerbated by any further increase (Grade 2C). We give fentanyl 3 mcg/kg intravenously [IV] over 30 to 60 seconds. Fentanyl should not be given to hypotensive patients or patients with hypovolemia who are dependent upon sympathetic drive to maintain blood pressure. (See 'Overview and approach' above and 'Lidocaine' above and 'Ultra-short acting opioid' above.)

●Induction agent for RSI – We suggest that etomidate (0.3 mg/kg IV push) be used as the induction agent for RSI in patients with elevated ICP (Grade 2C). Ketamine (1 to 2 mg/kg IV) may be used in hypotensive or normotensive patients. For patients with elevated ICP who are at no risk of hypotension, methohexital may be used. (See "Induction agents for rapid sequence intubation in adults for emergency medicine and critical care".)

●Neuromuscular blocking agent for RSI – We suggest that succinylcholine (1.5 mg/kg IV) be used as the neuromuscular blocking agent (NMBA) for RSI in patients with elevated ICP (Grade 2C). We prefer succinylcholine because of its rapid onset, consistent and reliable effects, and short duration of action. Contraindications to succinylcholine are listed in the text. Nondepolarizing (ie, competitive) NMBAs such as rocuronium do not cause an elevation of ICP and can also be used for RSI in this setting. (See 'Choice of neuromuscular blocking agent for RSI' above and "Neuromuscular blocking agents (NMBAs) for rapid sequence intubation in adults for emergency medicine and critical care".)

●Post-intubation monitoring – We suggest that all patients with elevated ICP who are intubated be monitored using continuous capnography in order to avoid inadvertent hypocapnia (pCO2 <35). (See 'Initiating mechanical ventilation' above.)

  1. Perkins ZB, Wittenberg MD, Nevin D, et al. The relationship between head injury severity and hemodynamic response to tracheal intubation. J Trauma Acute Care Surg 2013; 74:1074.
  2. Muller MD, Mast JL, Cui J, et al. Tactile stimulation of the oropharynx elicits sympathoexcitation in conscious humans. J Appl Physiol (1985) 2013; 115:71.
  3. Kayhan Z, Aldemir D, Mutlu H, Oğüş E. Which is responsible for the haemodynamic response due to laryngoscopy and endotracheal intubation? Catecholamines, vasopressin or angiotensin? Eur J Anaesthesiol 2005; 22:780.
  4. Takahashi S, Mizutani T, Miyabe M, Toyooka H. Hemodynamic responses to tracheal intubation with laryngoscope versus lightwand intubating device (Trachlight) in adults with normal airway. Anesth Analg 2002; 95:480.
  5. Shribman AJ, Smith G, Achola KJ. Cardiovascular and catecholamine responses to laryngoscopy with and without tracheal intubation. Br J Anaesth 1987; 59:295.
  6. Stoelting RK. Circulatory changes during direct laryngoscopy and tracheal intubation: influence of duration of laryngoscopy with or without prior lidocaine. Anesthesiology 1977; 47:381.
  7. Tewari P, Gupta D, Kumar A, Singh U. Opioid sparing during endotracheal intubation using McCoy laryngoscope in neurosurgical patients: the comparison of haemodynamic changes with Macintosh blade in a randomized trial. J Postgrad Med 2005; 51:260.
  8. Barak M, Ziser A, Greenberg A, et al. Hemodynamic and catecholamine response to tracheal intubation: direct laryngoscopy compared with fiberoptic intubation. J Clin Anesth 2003; 15:132.
  9. Tong JL, Ashworth DR, Smith JE. Cardiovascular responses following laryngoscope assisted, fibreoptic orotracheal intubation. Anaesthesia 2005; 60:754.
  10. Moorthy SS, Greenspan CD, Dierdorf SF, Hillier SC. Increased cerebral and decreased femoral artery blood flow velocities during direct laryngoscopy and tracheal intubation. Anesth Analg 1994; 78:1144.
  11. Chraemmer-Jørgensen B, Høilund-Carlsen PF, Marving J, Christensen V. Lack of effect of intravenous lidocaine on hemodynamic responses to rapid sequence induction of general anesthesia: a double-blind controlled clinical trial. Anesth Analg 1986; 65:1037.
  12. Moulton C, Pennycook AG. Relation between Glasgow coma score and cough reflex. Lancet 1994; 343:1261.
  13. Chung KS, Sinatra RS, Halevy JD, et al. A comparison of fentanyl, esmolol, and their combination for blunting the haemodynamic responses during rapid-sequence induction. Can J Anaesth 1992; 39:774.
  14. Cork RC, Weiss JL, Hameroff SR, Bentley J. Fentanyl preloading for rapid-sequence induction of anesthesia. Anesth Analg 1984; 63:60.
  15. Dahlgren N, Messeter K. Treatment of stress response to laryngoscopy and intubation with fentanyl. Anaesthesia 1981; 36:1022.
  16. Splinter WM, Cervenko F. Haemodynamic responses to laryngoscopy and tracheal intubation in geriatric patients: effects of fentanyl, lidocaine and thiopentone. Can J Anaesth 1989; 36:370.
  17. Hussain AM, Sultan ST. Efficacy of fentanyl and esmolol in the prevention of haemodynamic response to laryngoscopy and endotracheal intubation. J Coll Physicians Surg Pak 2005; 15:454.
  18. Adachi YU, Satomoto M, Higuchi H, Watanabe K. Fentanyl attenuates the hemodynamic response to endotracheal intubation more than the response to laryngoscopy. Anesth Analg 2002; 95:233.
  19. del Río Vellosillo M, Gallego García J, Soliveres Ripoll J, et al. [Bolus administration of fentanyl vs continuous perfusion of remifentanil for control of hemodynamic response to laryngoscopy and orotracheal intubation: a randomized double-blind trial]. Rev Esp Anestesiol Reanim 2009; 56:287.
  20. Payne KA, Murray WB, Oosthuizen JH. Obtunding the sympathetic response to intubation. Experience at 2 minutes after administration of the test agent in patients with cerebral aneurysms. S Afr Med J 1988; 73:584.
  21. Robinson N, Clancy M. In patients with head injury undergoing rapid sequence intubation, does pretreatment with intravenous lignocaine/lidocaine lead to an improved neurological outcome? A review of the literature. Emerg Med J 2001; 18:453.
  22. Butler J, Jackson R. Towards evidence based emergency medicine: best BETs from Manchester Royal Infirmary. Lignocaine premedication before rapid sequence induction in head injuries. Emerg Med J 2002; 19:554.
  23. Helfman SM, Gold MI, DeLisser EA, Herrington CA. Which drug prevents tachycardia and hypertension associated with tracheal intubation: lidocaine, fentanyl, or esmolol? Anesth Analg 1991; 72:482.
  24. Abou-Madi MN, Keszler H, Yacoub JM. Cardiovascular reactions to laryngoscopy and tracheal intubation following small and large intravenous doses of lidocaine. Can Anaesth Soc J 1977; 24:12.
  25. Bachofen M. [Suppression of blood pressure increases during intubation: lidocaine or fentanyl?]. Anaesthesist 1988; 37:156.
  26. Grover VK, Reddy GM, Kak VK, Singh S. Intracranial pressure changes with different doses of lignocaine under general anaesthesia. Neurol India 1999; 47:118.
  27. White PF, Schlobohm RM, Pitts LH, Lindauer JM. A randomized study of drugs for preventing increases in intracranial pressure during endotracheal suctioning. Anesthesiology 1982; 57:242.
  28. Donegan MF, Bedford RF. Intravenously administered lidocaine prevents intracranial hypertension during endotracheal suctioning. Anesthesiology 1980; 52:516.
  29. Bilotta F, Branca G, Lam A, et al. Endotracheal lidocaine in preventing endotracheal suctioning-induced changes in cerebral hemodynamics in patients with severe head trauma. Neurocrit Care 2008; 8:241.
  30. Samaha T, Ravussin P, Claquin C, Ecoffey C. [Prevention of increase of blood pressure and intracranial pressure during endotracheal intubation in neurosurgery: esmolol versus lidocaine]. Ann Fr Anesth Reanim 1996; 15:36.
  31. Yano M, Nishiyama H, Yokota H, et al. Effect of lidocaine on ICP response to endotracheal suctioning. Anesthesiology 1986; 64:651.
  32. Raymondos K, Münte S, Krauss T, et al. Cortical activity assessed by Narcotrend in relation to haemodynamic responses to tracheal intubation at different stages of cortical suppression and reflex control. Eur J Anaesthesiol 2003; 20:44.
  33. Oda Y, Nishikawa K, Hase I, Asada A. The short-acting beta1-adrenoceptor antagonists esmolol and landiolol suppress the bispectral index response to tracheal intubation during sevoflurane anesthesia. Anesth Analg 2005; 100:733.
  34. Feng CK, Chan KH, Liu KN, et al. A comparison of lidocaine, fentanyl, and esmolol for attenuation of cardiovascular response to laryngoscopy and tracheal intubation. Acta Anaesthesiol Sin 1996; 34:61.
  35. Clancy M, Halford S, Walls R, Murphy 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; 18:373.
  36. Moss E, Powell D, Gibson RM, McDowall DG. Effect of etomidate on intracranial pressure and cerebral perfusion pressure. Br J Anaesth 1979; 51:347.
  37. Modica PA, Tempelhoff R. Intracranial pressure during induction of anaesthesia and tracheal intubation with etomidate-induced EEG burst suppression. Can J Anaesth 1992; 39:236.
  38. Chesnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma 1993; 34:216.
  39. May N, Anderson K. Towards evidence based emergency medicine: best BETs from the Manchester Royal Infirmary. BET 3: Suxamethonium (succinylcholine) for RSI and intubation in head injury. Emerg Med J 2012; 29:511.
  40. Lanier WL, Iaizzo PA, Milde JH. Cerebral function and muscle afferent activity following intravenous succinylcholine in dogs anesthetized with halothane: the effects of pretreatment with a defasciculating dose of pancuronium. Anesthesiology 1989; 71:87.
  41. Cottrell JE, Hartung J, Giffin JP, Shwiry B. Intracranial and hemodynamic changes after succinylcholine administration in cats. Anesth Analg 1983; 62:1006.
  42. Kovarik WD, Mayberg TS, Lam AM, et al. Succinylcholine does not change intracranial pressure, cerebral blood flow velocity, or the electroencephalogram in patients with neurologic injury. Anesth Analg 1994; 78:469.
  43. Sun HL, Wu TJ, Ng CC, et al. Efficacy of oropharyngeal lidocaine instillation on hemodynamic responses to orotracheal intubation. J Clin Anesth 2009; 21:103.
  44. Warner KJ, Cuschieri J, Copass MK, et al. The impact of prehospital ventilation on outcome after severe traumatic brain injury. J Trauma 2007; 62:1330.
  45. Carney N, Totten AM, O'Reilly C, et al. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery 2017; 80:6.
Topic 266 Version 24.0

References

1 : The relationship between head injury severity and hemodynamic response to tracheal intubation.

2 : Tactile stimulation of the oropharynx elicits sympathoexcitation in conscious humans.

3 : Which is responsible for the haemodynamic response due to laryngoscopy and endotracheal intubation? Catecholamines, vasopressin or angiotensin?

4 : Hemodynamic responses to tracheal intubation with laryngoscope versus lightwand intubating device (Trachlight) in adults with normal airway.

5 : Cardiovascular and catecholamine responses to laryngoscopy with and without tracheal intubation.

6 : Circulatory changes during direct laryngoscopy and tracheal intubation: influence of duration of laryngoscopy with or without prior lidocaine.

7 : Opioid sparing during endotracheal intubation using McCoy laryngoscope in neurosurgical patients: the comparison of haemodynamic changes with Macintosh blade in a randomized trial.

8 : Hemodynamic and catecholamine response to tracheal intubation: direct laryngoscopy compared with fiberoptic intubation.

9 : Cardiovascular responses following laryngoscope assisted, fibreoptic orotracheal intubation.

10 : Increased cerebral and decreased femoral artery blood flow velocities during direct laryngoscopy and tracheal intubation.

11 : Lack of effect of intravenous lidocaine on hemodynamic responses to rapid sequence induction of general anesthesia: a double-blind controlled clinical trial.

12 : Relation between Glasgow coma score and cough reflex.

13 : A comparison of fentanyl, esmolol, and their combination for blunting the haemodynamic responses during rapid-sequence induction.

14 : Fentanyl preloading for rapid-sequence induction of anesthesia.

15 : Treatment of stress response to laryngoscopy and intubation with fentanyl.

16 : Haemodynamic responses to laryngoscopy and tracheal intubation in geriatric patients: effects of fentanyl, lidocaine and thiopentone.

17 : Efficacy of fentanyl and esmolol in the prevention of haemodynamic response to laryngoscopy and endotracheal intubation.

18 : Fentanyl attenuates the hemodynamic response to endotracheal intubation more than the response to laryngoscopy.

19 : [Bolus administration of fentanyl vs continuous perfusion of remifentanil for control of hemodynamic response to laryngoscopy and orotracheal intubation: a randomized double-blind trial].

20 : Obtunding the sympathetic response to intubation. Experience at 2 minutes after administration of the test agent in patients with cerebral aneurysms.

21 : In patients with head injury undergoing rapid sequence intubation, does pretreatment with intravenous lignocaine/lidocaine lead to an improved neurological outcome? A review of the literature.

22 : Towards evidence based emergency medicine: best BETs from Manchester Royal Infirmary. Lignocaine premedication before rapid sequence induction in head injuries.

23 : Which drug prevents tachycardia and hypertension associated with tracheal intubation: lidocaine, fentanyl, or esmolol?

24 : Cardiovascular reactions to laryngoscopy and tracheal intubation following small and large intravenous doses of lidocaine.

25 : [Suppression of blood pressure increases during intubation: lidocaine or fentanyl?].

26 : Intracranial pressure changes with different doses of lignocaine under general anaesthesia.

27 : A randomized study of drugs for preventing increases in intracranial pressure during endotracheal suctioning.

28 : Intravenously administered lidocaine prevents intracranial hypertension during endotracheal suctioning.

29 : Endotracheal lidocaine in preventing endotracheal suctioning-induced changes in cerebral hemodynamics in patients with severe head trauma.

30 : [Prevention of increase of blood pressure and intracranial pressure during endotracheal intubation in neurosurgery: esmolol versus lidocaine].

31 : Effect of lidocaine on ICP response to endotracheal suctioning.

32 : Cortical activity assessed by Narcotrend in relation to haemodynamic responses to tracheal intubation at different stages of cortical suppression and reflex control.

33 : The short-acting beta1-adrenoceptor antagonists esmolol and landiolol suppress the bispectral index response to tracheal intubation during sevoflurane anesthesia.

34 : A comparison of lidocaine, fentanyl, and esmolol for attenuation of cardiovascular response to laryngoscopy and tracheal intubation.

35 : 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.

36 : Effect of etomidate on intracranial pressure and cerebral perfusion pressure.

37 : Intracranial pressure during induction of anaesthesia and tracheal intubation with etomidate-induced EEG burst suppression.

38 : The role of secondary brain injury in determining outcome from severe head injury.

39 : Towards evidence based emergency medicine: best BETs from the Manchester Royal Infirmary. BET 3: Suxamethonium (succinylcholine) for RSI and intubation in head injury.

40 : Cerebral function and muscle afferent activity following intravenous succinylcholine in dogs anesthetized with halothane: the effects of pretreatment with a defasciculating dose of pancuronium.

41 : Intracranial and hemodynamic changes after succinylcholine administration in cats.

42 : Succinylcholine does not change intracranial pressure, cerebral blood flow velocity, or the electroencephalogram in patients with neurologic injury.

43 : Efficacy of oropharyngeal lidocaine instillation on hemodynamic responses to orotracheal intubation.

44 : The impact of prehospital ventilation on outcome after severe traumatic brain injury.

45 : Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition.

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