ISSN: 2455-3476

Global Journal of Anesthesiology

Editorial       Open Access      Peer-Reviewed

Intravenous General Anesthesia for Patients with Neurological Disorders

Kentaro Ouchi*

Department of Dental Anesthesiology, Assistant professor, Field of Maxillofacial Diagnostic and Surgical Sciences, Faculty of Dental Science, Kyushu University, Graduate School, Japan

Author and article information

*Corresponding author: Kentaro Ouchi, DDS, PhD, Department of Dental Anesthesiology, Field of Maxillofacial Diagnostic and Surgical Sciences, Faculty of Dental Science, Kyushu University Graduate School, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan, Tel: +81-92-641-1151; Fax: +81-92-642-6481; E-mail: [email protected]
doi : 10.17352/2455-3476.000018
Submitted: 14 October, 2015 | Accepted: 15 October, 2015 | Published: 15 October, 2015
Keywords: Intravenous General Anesthesia for Patients with Neurological Disorders; Mechanism; Clinical application; Evidence; Cooling methods; Practical aspects

Cite this as

Ouchi K (2015) Intravenous General Anesthesia for Patients with Neurological Disorders. Glob J Anesth. 2015; 2(2): 54-56. Available from: 10.17352/2455-3476.000018

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© 2015 Ouchi K. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

In dental practice, intravenous general anesthesia is useful for patients who are difficult to treat when not sedated such as those with neurological disorders [1].

Indexing and Abstracting

Editorial

In dental practice, intravenous general anesthesia is useful for patients who are difficult to treat when not sedated such as those with neurological disorders [[4], continuous intravenous infusion of propofol was initiated using the TCI method. The dose of propofol was titrated to achieve a BIS of 50 and achieve an adequate level of anesthesia: asleep but not responding to stimulation. Endotracheal intubation was not performed, and spontaneous breathing was maintained. The level of anesthesia was maintained at BIS 30-50 by adjusting the target propofol level using TCI (Figure 1). Without BIS, The dose of propofol was titrated to achieve a Mackenzie Grant score of 5 and to achieve an adequate level of anesthesia: asleep, but not responding to stimulation. The level of anesthesia was maintained at a Mackenzie and Grant score of 5 by adjusting the target propofol level using the propofol TCI (Figure 2). If respiratory depression was observed or BIS value was less than 30, the target blood concentration of propofol was decreased by 0.2 μg/ml. If the anesthesia level was deemed inadequate BIS value was more than 50, the target blood level of propofol was increased by 0.2 μg/ml. The dental procedure was started after the anesthesia level became stable without respiratory depression. A local anesthetic was used appropriately by the operating dentist. Administration of propofol was discontinued at the end of the dental procedure. Patients were monitored until recovery from anesthesia, when they were fully awake and had stable respiration.

Figure 1: Intravenous general anesthesia protocol with BIS. TCI: target-controlled infusion. BIS: Bispectral index.
Figure 2: Intravenous general anesthesia protocol without BIS.

Antiepileptics affect for anesthesia

Patients with intellectual disabilities need higher doses of sedatives than those without intellectual disabilities to obtain an adequate level of anesthesia [[6]. Many of neurological disorders patients have epilepsy and are medicated with antiepileptic drugs. In these reports, the group with lower doses of sedatives to obtain an adequate level included those who were given an antiepileptic. In patients not given an antiepileptic, there were no differences in the required dose of propofol and emergence among patients with autism, cerebral palsy, and intellectual disability [8]-[7].

Hepatic enzyme inhibition usually occurs because of competition at the enzyme site and results in a decrease in the rate of metabolism of the affected drug [[12]. Thus, certain antiepileptic drugs have been increased the blood concentration of propofol by inhibiting the action of CYP and UGT. Carbamazepine contributes to the competitive inhibition of hepatic CYP2C9, because metabolism CYP is the same as propofol.(7) In addition, carbamazepine inhibits 2C19 [[7]. In addition, valproate inhibits CYP2C9 in vitro [15]. And valproate inhibits UGT 1A9, which mediates glucuronic acid conjugation, the main metabolic pathway of propofol [20],[17],22]. But, phenobarbital induces CYP2C19 [[24]. But, it is reported that zonisamide does not induce or inhibit the metabolism of other drugs that included drugs metabolize by CYP3A4 or CYP2C19 [2525. Sills G, Brodie M (2007) Pharmacokinetics and drug interactions with zonisamide. Epilepsia 48: 435-441.]. Therefore, zonisamide may not affect the metabolism of propofol.

Therefore, propofol metabolism is affected by antiepileptic use, and is affected by the type of antiepileptic (Table 1). Consequently, in intravenous anesthesia for patients with epilepsy, required propofol dose is lower, emergence from anesthesia is delayed.

Table 1: Affect for propofol metabolism.
Antiepileptic Affect for propofol metabolism
Carbamazepine Inhibit
Valproate Inhibit
Phenobarbital Induce / Inhibit
Phenytoin Inhibit
Zonisamide No affect
Benzodiazepine Inhibit
Topiramate Inhibit

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