Department of Dental Anesthesiology, Assistant professor, Field of Maxillofacial Diagnostic and Surgical Sciences, Faculty of Dental Science, Kyushu University, Graduate School, Japan
Received: 14 October, 2015 Accepted: 15 October, 2015 Published: 15 October, 2015
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:
Ouchi K (2015) Intravenous General Anesthesia for Patients with Neurological Disorders. Glob J Anesthesiol 2(2): 054-056. DOI: 10.17352/2455-3476.000018
© 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.
In dental practice, intravenous general anesthesia is useful for patients who are difficult to treat when not sedated such as those with neurological disorders [11. Manley MC, Skelly AM, Hamilton AG (2000) Dental treatment for people with challenging behaviour: general anaesthesia or sedation? British dental journal 188: 358-360.].
A bispectral index sensor (BIS) was attached to the patient's forehead and connected to a BIS monitor (Aspect Medical Systems Inc.) to evaluate the level of intravenous general anesthesia. BIS is nonessential but helpful. In intravenous anesthesia without BIS, observation of sedation score is necessary, more precisely. Pulse oximetry sensor placed on the patient's digit. Pulse oximetry is usually used for monitoring of respiratory function during intravenous anesthesia. However, it has certain limitations. Under anesthesia with oxygen supplementation, the decrease in pulse oxygen saturation may be delayed despite severe respiratory insufficiency [22. Keidan I, Gravenstein D, Berkenstadt H, Ziv A, Shavit I, et al. (2008) Supplemental oxygen compromises the use of pulse oximetry for detection of apnea and hypoventilation during sedation in simulated pediatric patients. Pediatrics 122: 293-298.,33. Fu ES, Downs JB, Schweiger JW, Miguel RV, Smith RA (2004) Supplemental oxygen impairs detection of hypoventilation by pulse oximetry. Chest 126:1552-1558.]. Respiratory rate measurement involved use of an adhesive sensor, including an acoustic transducer (Masimo Corp., Tokyo, Japan), placed on the patient's throat, on the side of the larynx and above the thyroid cartilage. The sensor allows real time analysis of the vibrations emanating from the patient's larynx and enables isolation of the respiratory sounds via analysis of the trace obtained through various filters. The acoustic signal is then converted to a numerical value, allowing a continuous display of the respiratory rate value. Respiratory rate measurement is nonessential but helpful. In intravenous anesthesia without respiratory rate measurement, observation of oxygen saturation and movement of the chest by the breathing is necessary, more precisely.
Intravenous general anesthesia protocol
Oxygen supplied through nasal cannula. Nitrous oxide (approximate concentration, 20%) can also be used together for oxygen supplementation. Intravenous general anesthesia was induced and maintained with continuous infusion of propofol. Using a propofol TCI pump (Graseby Medical Ltd., Hertfordshire, UK, or Terumo Co., Tokyo, Japan) with a built-in TCI system (Diprifusor, AstraZeneca Plc., London, UK) and according to the parameters reported by Marsh [44. Marsh B, White M, Morton N, Kenny GN (1991) Pharmacokinetic model driven infusion of propofol in children. British journal of anaesthesia 67: 41-48.], 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.
- Manley MC, Skelly AM, Hamilton AG (2000) Dental treatment for people with challenging behaviour: general anaesthesia or sedation? British dental journal 188: 358-360 .
- Keidan I, Gravenstein D, Berkenstadt H, Ziv A, Shavit I, et al. (2008) Supplemental oxygen compromises the use of pulse oximetry for detection of apnea and hypoventilation during sedation in simulated pediatric patients. Pediatrics 122: 293-298 .
- Fu ES, Downs JB, Schweiger JW, Miguel RV, Smith RA (2004) Supplemental oxygen impairs detection of hypoventilation by pulse oximetry. Chest 126:1552-1558 .
- Marsh B, White M, Morton N, Kenny GN (1991) Pharmacokinetic model driven infusion of propofol in children. British journal of anaesthesia 67: 41-48 .
- Miyawaki T, Kohjitani A, Maeda S, Egusa M, Mori T, et al. (2004) Intravenous sedation for dental patients with intellectual disability. Journal of intellectual disability research : JIDR 48: 764-768 .
- Asahi Y, Kubota K, Omichi S (2009) Dose requirements for propofol anaesthesia for dental treatment for autistic patients compared with intellectually impaired patients. Anaesthesia and intensive care 37: 70-73 .
- Ouchi K, Sugiyama K (2015) Required propofol dose for anesthesia and time to emerge are affected by the use of antiepileptics: prospective cohort study. BMC Anesthesiol 15: 34 .
- Oda Y, Hamaoka N, Hiroi T, Imaoka S, Hase I, et al. (2001) Involvement of human liver cytochrome P4502B6 in the metabolism of propofol. Br J Clin Pharmacol 51: 281-285 .
- Court MH, Duan SX, Hesse LM, Venkatakrishnan K, Greenblatt DJ (2001) Cytochrome P-450 2B6 is responsible for interindividual variability of propofol hydroxylation by human liver microsomes. Anesthesiology 94: 110-119.
- Guitton J, Buronfosse T, Desage M, Flinois JP, Perdrix JP, et al. (1998) Possible involvement of multiple human cytochrome P450 isoforms in the liver metabolism of propofol. Br J Anaesth 80: 788-795 .
- Perucca E (2002) Pharmacological and therapeutic properties of valproate: a summary after 35 years of clinical experience. CNS drugs 16: 695-714 .
- Anderson GD (1998) A mechanistic approach to antiepileptic drug interactions. Ann Pharmacother. 32: 554-563.
- Yap KY, Chui WK, Chan A (2008) Drug interactions between chemotherapeutic regimens and antiepileptics. Clin Ther. 30: 1385-1307 .
- Sachdeo RC, Sachdeo SK, Levy RH, Streeter AJ, Bishop FE, et al. (2002) Topiramate and phenytoin pharmacokinetics during repetitive monotherapy and combination therapy to epileptic patients. Epilepsia 43: 691-696 .
- Wen X, Wang JS, Kivisto KT, Neuvonen PJ, Backman JT (2001) In vitro evaluation of valproic acid as an inhibitor of human cytochrome P450 isoforms: preferential inhibition of cytochrome P450 2C9 (CYP2C9). Br J Clin Pharmacol 52: 547-553 .
- Ethell BT, Anderson GD, Burchell B (2003) The effect of valproic acid on drug and steroid glucuronidation by expressed human UDP-glucuronosyltransferases. Biochem Pharmacol 65: 1441-1449 .
- Mutlib AE, Goosen TC, Bauman JN, Williams JA, Kulkarni S, et al. (2006) Kinetics of acetaminophen glucuronidation by UDP-glucuronosyltransferases 1A1, 1A6, 1A9 and 2B15. Potential implications in acetaminophen-induced hepatotoxicity. Chem Res Toxicol 19: 701-709 .
- Levy RH BM (1995) Phenytoin: interactions with other drugs: mechanistic aspects. In: Levy RH MR, Meldrum BS editor. Antiepileptic drugs. Volume. 4 ed. New York: Raven Press 329-344.
- Walzer M, Bekersky I, Blum RA, Tolbert D (2012) Pharmacokinetic drug interactions between clobazam and drugs metabolized by cytochrome P450 isoenzymes. Pharmacotherapy 32: 340-353 .
- Sankar R (2012) GABA(A) receptor physiology and its relationship to the mechanism of action of the 1,5-benzodiazepine clobazam. CNS drugs 26: 229-244 .
- Wheless JW, Phelps SJ (2013) Clobazam: a newly approved but well-established drug for the treatment of intractable epilepsy syndromes. J Child Neurol 28: 219-229 .
- Kostrubsky SE, Sinclair JF, Strom SC, Wood S, Urda E, et al. (2005) Phenobarbital and phenytoin increased acetaminophen hepatotoxicity due to inhibition of UDP-glucuronosyltransferases in cultured human hepatocytes. Toxicol Sci 87: 146-155 .
- Zhou SF, Zhou ZW, Yang LP, Cai JP (2009) Substrates, inducers, inhibitors and structure-activity relationships of human Cytochrome P450 2C9 and implications in drug development. Curr Med Chem 16: 3480-3675 .
- Nakasa H, Nakamura H, Ono S, Tsutsui M, Kiuchi M, et al. (1998) Prediction of drug-drug interactions of zonisamide metabolism in humans from in vitro data. Eur J Clin Pharmacol 54: 177-183 .
- Sills G, Brodie M (2007) Pharmacokinetics and drug interactions with zonisamide. Epilepsia 48: 435-441 .