Induction and Emergence / Extubation in Neurosurgical patients: Tricks and Tips

Dr Deepak Madankar
Dr Deepak Madankar

Dr Deepak Madankar
MD (Anaesthesiology), FCCS, ENLS
Chief Consultant –Dept. of Anaesthesia and pain medicine, MEDITRINA Institute of Medical Sciences, Ramdaspeth, Nagpur, INDIA.

Anesthesia for neurosurgical procedures requires balanced anesthesia with smooth induction and emergence. The fundamental necessities in neuroanesthesia include maintenance of adequate cerebral perfusion pressure (CPP), avoidance of intracranial hypertension, and the provision of optimal surgical conditions to avoid further progression of the pre-existing neurological insult.1 

The patients having intracranial pathology especially space occupying lesions in brain and Traumatic brain injury (TBI) are usually in a state of delicate intracranial homeostasis. Understanding the pathophysiology of cerebral hypertension and the systemic/cerebral physiological effects of various induction agents is important while making a choice of a particular anesthetic agent. The assessment of the level of intracranial pressure (ICP) relies clinically on the Glasgow coma score. ICP is assessed by measuring it directly by various available techniques (fluid-filled transduced ventriculostomy, fiberoptic sensors, microchips etc.) and with the help of signs of ICH on the CT-scan and transcranial doppler examination. The main concern in managing patients with intracranial hypertension (ICH) is to maintain the cerebral perfusion pressure (CPP) and oxygenation. Therefore, emphasis should be placed upon the avoidance of cerebral ischemia and hypoxia when choosing anesthetic induction agents.

Cerebral autoregulation normally serves to prevent MAP related increase in CBV. As the cerebral circulation constricts to maintain a constant CBF in the face of a rising MAP, CBV actually decreases 2. In patients with neurological pathology where autoregulation is impaired or the upper limit (~ 150 mmHg) is exceeded, CBF and eventually CBV increase in parallel to arterial pressure rise. Subsequently a declining MAP causes cerebral vasodilatation to maintain a constant flow resulting in progressive increase in CBV. Thus exaggerated increase in CBV occurs as MAP falls below the lower limit of autoregulation. This increase in CBV in the face of falling MAP is the principal reason for ICP increase.1 In healthy subjects initial increase in CBV does not result in significant ICP elevation but after exhaustion of compensatory adjustment by other intracranial components, reduction in intracranial compliance occurs and further increase in CBV can cause steep increase in ICP and brain herniation or may reduce CPP sufficiently to cause ischaemia.

Various maneuvers during induction of anaesthesia like laryngoscopy and endotracheal intubation may produce deleterious effects on mean arterial pressure (MAP), intracranial pressure (ICP) & therefore on cerebral perfusion pressure (CPP). The control and manipulation of cerebral blood flow (CBF) are of utmost importance to the management of ICP during anaesthesia because CBF varies according to vasoconstrictor – vasodilator response of anaesthetic agent. There is no particular single recommended anaesthetic technique for patients with ICH. Various factors which might be of relevance during anaesthetic induction in patients of raised intracranial tension are:

Intravenous Verses inhalational anesthetic induction- Theoretically, intravenous anaesthesia is a better choice than inhalation anesthesia because of the cerebral vasodilatation induced by inhalation agents. Intravenous anaesthetics in general, cause a decrease in CBF and cerebral metabolic rate of oxygen (CMRO2). The decrease in CBF induced by most of the intravenous anaesthetics appears to be the result of decreased cerebral metabolism secondary to cerebral functional depression. Thiopentone causes dose dependent depression of CMRO2 and a parallel reduction in CBF & ICP. ICP is decreased proportionally more than MAP. Therefore CPP remains un-compromised. This is particularly beneficial for patients with increased ICP making thiopentone an appropriate drug during induction of anaesthesia in neurosurgery.3

Propofol is one of the most common and popular intravenous induction agent used in modern anaesthetic practice. Propofol controls elevated ICP and maintain CPP. The most significant benefit of propofol administration is the maintenance of cerebral auto-regulation and response to carbon dioxide within normal levels although adverse effects such as myoclonus, apnea, hypotension and rare occasions of local thrombophlebitis may occur. Treatment of hypovolaemia with fluid loading and the early use of vasoactive agents can be recommended to maintain CPP. Studies have demonstrated that anaesthetic induction using propofol produces a decrease in CSF pressure similar in magnitude and duration to that found with thiopentone.4,5 Etomidate (0.2-0.3 mg/kg) or midazolam (0.2-0.4 mg/kg) are some of the other agents, which may help provide a more hemodynamically stable induction.

Volatile anaesthetics produce cerebral vasodilation and thus result in raised ICP. However, studies have shown that this increase in ICP may be insignificant in space occupying lesion in both adults and children if the anaesthetic concentration is kept below 1.2 MAC 6-8.Inhalational induction is usually reserved for children. The choice between inhalation induction and intravenous induction is dictated by the presence or absence of intravenous access, the patient’s neurological status, any coexisting disease processes, and the child’s NPO status. Nitrous oxide is a potent cerebral vasodilator and may result in increased ICP in a dose dependent manner. The deliterious effects of nitrous oxide can be reduced when used in the background of opioids, propofol, benzodiazepines and to some extent with volatile anaesthetics. Nitrous oxide should better be avoided in patients with severe ICH or during emergency surgery.

Various other agents can be used along with both intravenous and inhalational agents for induction. These agents decrease ICP by various modes of action and also have a sparing effect of primary induction agent. Opiates are often recommended to blunt the response to DL and craniotomy. Morphine (0.1-0.15 mg/kg), Fentanyl (1-10 ucg/kg) and its derivatives may be used depending upon the type of surgical procedure, duration of analgesia required and availability. Lignocaine 1.5 mg/kg may help blunt the response to DL. Consider initiating hyperventilation immediately after induction (gives you a margin of safety in case DL is stimulating).

Dexmedetomidine, a selective α-2 agonist has been used as an adjuvant to IV anesthetic agents.9 It has gained its popularity recently due to its highly selective α2 agonist action that produces sympatholysis, sedation without respiratory depression.10 Dexmedetomidine reduces CBF in a dose-dependent manner79–81 has got opioid and anesthetic agent sparing properties with improved hemodynamic stability. Muscle relaxants should be used along with the induction agent to favor intubation preferably a non-depolarizing NMBD. Succinylcholine may cause transient increase in ICP during induction secondary to fasciculations, however succinylcholine is not contraindicated if rapid airway securement is warranted or difficult airway is likely. Post-intubation extra care needs to be taken in securing the airway as it will most likely be inaccessible later on during the intraoperative period.

The goal at the end of surgical procedure is to have a comfortable and pain free patient with avoidance of coughing to reduce the sudden fluctuations in blood pressure and ICP. The most feared complications after intracranial surgery are development of an intracranial hematoma and major cerebral edema. 11,12 These complications are deleterious and may result in cerebral hypo perfusion and brain injury. Arterial hypertension via catecholamine release or sympathetic stimulation and hypercapnia may be predisposing factors. Other systemic secondary insults to the brain such as hypoxia and hypotension may exacerbate neuronal injury in hypo perfused areas of the brain. Thus, the anesthetic emergence of a neurosurgical patient should include maintenance of stable respiratory and cardiovascular parameters.

Bucking and coughing causes sudden increase in intrathoracic pressure which is transmitted to arteries and veins. This transient increase in cerebral arterial and venous pressure results in various potential consequences like edema formation, bleeding, and elevation of intracranial pressure. Coughing is a specific concern in certain surgical procedures eg. Trans-sphenoidal pituitary surgery, where the dura and arachnoid membranes are opened and finally closed at the end of procedure. Coughing causes a sudden substantial increase in CSF pressure which may disrupt this closure and result in CSF leak. Minimal stimulation and reaction to the endotracheal tube prevents sympathetic stimulation and undue increase in venous pressure.

The intraoperative infusion of opioids if used should be tapered at the end of procedure and additional boluses of short acting opioids may be used for a smooth extubation. If the preoperative condition of the patient demands continuation of mechanical ventilation postoperatively, the patient should remain deeply sedated and paralysed to maintain ICP. Two strategies of emergence and extubation are usually employed by neuro-anaesthesiologists in operation theatre. A delayed one, where patient is extubated in the intensive care unit (ICU) after regaining complete sensorium and reflexes. This is recommended to achieve better thermal and cardiovascular stability after major intracranial procedures. Major operative procedures which involve handling of critical brain areas and increased ICP are usually considered for delayed emergence and extubation.

On the other hand, early on table emergence and extubation is favored by others for the timely diagnosis of neurosurgical complications, which is required to limit the brain damage. The diagnosis of complications relies on rapid neurological examination after early awakening. Early recovery and extubation in the operating room is the preferred method when the preoperative state of consciousness is relatively normal and surgery does not involve critical brain areas or extensive manipulation. Uncomplicated surgery is associated with minimal metabolic and hemodynamic changes; hence a good recovery can be expected in normothermic, normovolemic and hemodynamically stable patients. In the complicated or unstable patient, the risks of early extubation may outweigh the benefits. However, if required, a brief awakening of the patient without extubation to allow early neurological evaluation, followed by delayed emergence and extubation may be tried in these patients. Close hemodynamic and respiratory monitoring are mandatory in all cases. The availability of ultrashort intravenous anesthetic agents and adrenergic blocking agents has added to the flexibility in the management of smooth extubation during the emergence period after intracranial surgery.

Practical tips to reduce bucking on endotracheal tube and the consequent sympathetic stimulation resulting in deleterious effects of hypertension and increased ICP can be summarized as:

  1. Continuation of the volatile anesthetic till the end of stimulus and surgical procedure along with supplementation with small doses of propofol or ultrashort acting opioid or labetalol either by bolus or infusion.
  2. For rapid and smooth emergence, the last inhaled anesthetic to be withdrawn should be nitrous oxide (if at all used during the procedure) and should be discontinued after complete reversal of muscle relaxants.
  3. An anesthetic technique to include as much narcotic as is consistent with spontaneous ventilation at the conclusion of the procedure is recommended.
  4. Intravenous lignocaine 1.5 mg/kg, approximately 90 seconds before the head movement associated with applying the dressing and oral suction and extubation.
  5. Administration of vasoactive agents, most commonly labetalol and esmolol for managing systemic hypertension at the end of surgical procedure.13
  6. Other agents  like Ca channel antagonists, NTG, SNP are cerebral vasodilators hence generally not preferred.
  7. Administration of dexmedetomidine during the procedure also has been reported to reduce the hypertensive response to emergence.14
  8. Awake “no touch” extubation technique may be adopted in which patient is extubated, once the patient spontaneously wakes up along with gentle suction and minimal stimulation during emergence from general anesthesia.15



 1. Magni G, Baisi F, La Rosa I, et al. No difference in emergence time and early cognitive function between sevoflurane-fentanyl and propofol-remifentanil in patients undergoing craniotomy for supratentorial intracranial surgery. J Neurosurg Anesthesiol 2005;17(3):134–138     

2. Ferrari M, Wilson DA, Hanley DF, et al. Effect of graded hypotension on cerebral blood flow, blood volume& mean transit time in dogs. Am J Physiol 1992; 262: 1908-14. 

3. Albrecht RF, Miletich DJ, Rosenberg R, et al. Cerebral blood flow& metabolic changes from induction to onset of anesthesia with halothane& pentobarbital. Anesthesiology 1977; 47:252-­256.

4. Hartung HJ. Intracranial pressure after propofol and thiopen­tone administration in patients with severe head trauma. Anaes­thetist 1987; 36:285-287.     

5. Van – Hemelrijik J, Van Aken H, Plets C, et al. The effects of propofol on intracranial pressure and cerebral perfusion pressure in patients with brain tumors. Acta Anaesthesial Belg 1989; 40 : 95-100.

6. Sponheim S, Skraastad Ø, Helseth E, Due-Tønnesen B, Aamodt G, et al. (2003) Effects of 0.5 and 1.0 MAC isoflurane, sevoflurane and desflurane on intracranial and cerebral perfusion pressures in children. Acta Anaesthesiol Scand 47: 932-938.

7. Kaye A, Kucera IJ, Heavner J, Gelb A, Anwar M, et al. (2004) The comparative effects of desflurane and isoflurane on lumbar cerebrospinal fluid pressure in patients undergoing craniotomy for supratentorial tumors. Anesth Analg 98: 1127-1132, table of contents.

8. Fraga M, Rama-Maceiras P, Rodiño S, Aymerich H, Pose P, et al. (2003) The effects of isoflurane and desflurane on intracranial pressure,cerebral perfusion pressure, and cerebral arteriovenous oxygen content difference in normocapnic patients with supratentorial brain tumors. Anesthesiology 98: 1085-90.

9. Flower O, Hellings S. Sedation in traumatic brain injury. Emerg Med Int 2012;2012:637171

10. Candiotti KA, Bergese SD, Bokesch PM, Feldman MA, Wisemandle W, Bekker AY; MAC Study Group. Monitored anesthesia care with dexmedetomidine: a prospective, randomized, double-blind, multicenter trial. Anesth Analg 2010;110(1):47–56

11. Johansson B, Li CL, Olsson Y, et al: The effect of acute arterial hypertension on the blood-brain barrier to protein tracers.  Acta Neuropathol (Berl)  1970; 16:117-124.

12. Hatashita S, Hoff JT, Ishii S: Focal brain edema associated with acute arterial hypertension.  J Neurosurg  1986; 64:643-649.

13. Grillo P, Bruder N, Auquier P, et al: Esmolol blunts the cerebral blood flow velocity increase during emergence from anesthesia in neurosurgical patients.  Anesth Analg  2003; 96:1145-1149.

14. Tanskanen PE, Kytta JV, Randell TT, et al: Dexmedetomidine as an anaesthetic adjuvant in patients undergoing intracranial tumour surgery: A double-blind, randomized and placebo-controlled study.  Br J Anaesth  2006; 97:658-665.

15. The incidence of laryngospasm with a “no touch” extubation technique after tonsillectomy and adenoidectomy. Tsui BC1, Wagner A, Cave D, Elliott C, El-Hakim H, Malherbe S. Anesth Analg. 2004 Feb;98(2):327-9, table of contents.