The relationship between anti-seizures medications and metabolic acidosis in craniotomy operations: is topiramate or zonisamide the cause of metabolic acidosis?
Anti-seizures medications
Antiepileptic drugs
Craniotomy
Epilepsy
Metabolic acidosis
Topiramate
Zonisamide
Journal
BMC anesthesiology
ISSN: 1471-2253
Titre abrégé: BMC Anesthesiol
Pays: England
ID NLM: 100968535
Informations de publication
Date de publication:
27 Aug 2024
27 Aug 2024
Historique:
received:
31
03
2024
accepted:
08
08
2024
medline:
28
8
2024
pubmed:
28
8
2024
entrez:
27
8
2024
Statut:
epublish
Résumé
The most commonly prescribed anti-seizures medications (ASMs) for the treatment of epilepsy are currently topiramate, zonisamide, lacosamide, carbamazepine and levetiracetam. The objective of this study was to examine the correlation between preoperative, intraoperative, and postoperative metabolic acidosis and the use of ASMs prior to craniotomy operations. This retrospective cross-sectional study evaluated patients who underwent intracranial surgery with craniotomy under general anaesthesia between May 2020 and April 2023 and used ASMs. The patients were classified into four groups based on the pharmacological mechanisms of action of the ASMs administered before intracranial surgery (Group-I, zonisamide or topiramate; Group-II, lacosamide; Group-III, carbamazepine; Group-IV, levetiracetam). Metabolic acidosis severity was defined based on base excess (BE) levels: mild (-3 to -5), moderate (-5 to -10), and severe (below - 10). The study investigated the correlation between ASMs and the severity of metabolic acidosis in preoperative, intraoperative, and postoperative blood gas measurements. Out of 35 patients, 24 patients underwent intracranial surgery and 11 patients underwent epilepsy surgery. There were statistically significant differences in the severity of metabolic acidosis between preoperative (p < 0.001), intraoperative (p < 0.001) and postoperative (p = 0.01) groups. The preoperative mean BE of group-I was - 4.7, which was statistically lower than that of group-III (p = 0.01) and group-IV (p < 0.001). Intraoperatively and postoperatively, group-I had a mean BE of -7.5 and - 3.2, respectively, which was statistically lower than that of groups II (p = 0.007; p = 0.04), III (p = 0.002; p = 0.03), and IV (p < 0.001; p = 0.009). There was no statistically significant difference in BE between groups II, III and IV at all three time points. Group I had the lowest BE at all three time points. Intraoperative bicarbonate was administered to all patients in group I, whereas no intraoperative bicarbonate was required in the other groups. In group I, 50% of patients required postoperative intensive care. The use of ASMs in patients undergoing surgery is important in terms of mortality and morbidity. Topirimat and zonisamide are ASMs that can cause preoperative, intraoperative and postoperative metabolic acidosis. Patients receiving topirimat or zonisamide are particularly susceptible to metabolic acidosis. Special care should be taken in the management of anaesthesia in patients receiving these drugs, and monitoring of the perioperative metabolic status is essential.
Sections du résumé
BACKGROUND/AIM
OBJECTIVE
The most commonly prescribed anti-seizures medications (ASMs) for the treatment of epilepsy are currently topiramate, zonisamide, lacosamide, carbamazepine and levetiracetam. The objective of this study was to examine the correlation between preoperative, intraoperative, and postoperative metabolic acidosis and the use of ASMs prior to craniotomy operations.
MATERIALS AND METHODS
METHODS
This retrospective cross-sectional study evaluated patients who underwent intracranial surgery with craniotomy under general anaesthesia between May 2020 and April 2023 and used ASMs. The patients were classified into four groups based on the pharmacological mechanisms of action of the ASMs administered before intracranial surgery (Group-I, zonisamide or topiramate; Group-II, lacosamide; Group-III, carbamazepine; Group-IV, levetiracetam). Metabolic acidosis severity was defined based on base excess (BE) levels: mild (-3 to -5), moderate (-5 to -10), and severe (below - 10). The study investigated the correlation between ASMs and the severity of metabolic acidosis in preoperative, intraoperative, and postoperative blood gas measurements.
RESULTS
RESULTS
Out of 35 patients, 24 patients underwent intracranial surgery and 11 patients underwent epilepsy surgery. There were statistically significant differences in the severity of metabolic acidosis between preoperative (p < 0.001), intraoperative (p < 0.001) and postoperative (p = 0.01) groups. The preoperative mean BE of group-I was - 4.7, which was statistically lower than that of group-III (p = 0.01) and group-IV (p < 0.001). Intraoperatively and postoperatively, group-I had a mean BE of -7.5 and - 3.2, respectively, which was statistically lower than that of groups II (p = 0.007; p = 0.04), III (p = 0.002; p = 0.03), and IV (p < 0.001; p = 0.009). There was no statistically significant difference in BE between groups II, III and IV at all three time points. Group I had the lowest BE at all three time points. Intraoperative bicarbonate was administered to all patients in group I, whereas no intraoperative bicarbonate was required in the other groups. In group I, 50% of patients required postoperative intensive care.
CONCLUSION
CONCLUSIONS
The use of ASMs in patients undergoing surgery is important in terms of mortality and morbidity. Topirimat and zonisamide are ASMs that can cause preoperative, intraoperative and postoperative metabolic acidosis. Patients receiving topirimat or zonisamide are particularly susceptible to metabolic acidosis. Special care should be taken in the management of anaesthesia in patients receiving these drugs, and monitoring of the perioperative metabolic status is essential.
Identifiants
pubmed: 39192186
doi: 10.1186/s12871-024-02677-5
pii: 10.1186/s12871-024-02677-5
doi:
Substances chimiques
Zonisamide
459384H98V
Topiramate
0H73WJJ391
Anticonvulsants
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
296Informations de copyright
© 2024. The Author(s).
Références
Fisher RS, Acevedo C, Arzimanoglou A, Bogacz A, Cross JH, Elger CE, Engel J Jr., Forsgren L, French JA, Glynn M, et al. ILAE official report: a practical clinical definition of epilepsy. Epilepsia. 2014;55(4):475–82.
doi: 10.1111/epi.12550
pubmed: 24730690
Rugg-Gunn F, Miserocchi A, McEvoy A. Epilepsy surgery. Pract Neurol. 2020;20(1):4–14.
pubmed: 31420415
Hakami T. Neuropharmacology of antiseizure drugs. Neuropsychopharmacol Rep. 2021;41(3):336–51.
doi: 10.1002/npr2.12196
pubmed: 34296824
pmcid: 8411307
Winum JY, Poulsen SA, Supuran CT. Therapeutic applications of glycosidic carbonic anhydrase inhibitors. Med Res Rev. 2009;29(3):419–35.
doi: 10.1002/med.20141
pubmed: 19058143
Temperini C, Innocenti A, Scozzafava A, Parkkila S, Supuran CT. The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors. J Med Chem. 2010;53(2):850–4.
doi: 10.1021/jm901524f
pubmed: 20028100
Mirza NS, Alfirevic A, Jorgensen A, Marson AG, Pirmohamed M. Metabolic acidosis with topiramate and zonisamide: an assessment of its severity and predictors. Pharmacogenet Genomics. 2011;21(5):297–302.
doi: 10.1097/FPC.0b013e3283441b95
pubmed: 21278619
Philippi H, Boor R, Reitter B. Topiramate and metabolic acidosis in infants and toddlers. Epilepsia. 2002;43(7):744–7.
doi: 10.1046/j.1528-1157.2002.37201.x
pubmed: 12102678
Ozer Y, Altunkaya H. Topiramate induced metabolic acidosis. Anaesthesia. 2004;59(8):830–830.
doi: 10.1111/j.1365-2044.2004.03884.x
pubmed: 15270982
Burmeister JE, Pereira RR, Hartke EM, Kreuz M. Topiramate and severe metabolic acidosis: case report. Arq Neuropsiquiatr. 2005;63(2B):532–4.
doi: 10.1590/S0004-282X2005000300032
pubmed: 16059613
Sills GJ, Rogawski MA. Mechanisms of action of currently used antiseizure drugs. Neuropharmacology. 2020;168:107966.
doi: 10.1016/j.neuropharm.2020.107966
pubmed: 32120063
Waters JH, Miller LR, Clack S, Kim JV. Cause of metabolic acidosis in prolonged surgery. Crit Care Med. 1999;27(10):2142–6.
doi: 10.1097/00003246-199910000-00011
pubmed: 10548196
Fleisher LA, Roizen MF, Roizen J. Essence of Anesthesia Practice E-Book. Elsevier Health Sciences; 2017.
Türe H, Keskin Ö, Çakır Ü, Aykut Bingöl C, Türe U. The frequency and severity of metabolic acidosis related to topiramate. J Int Med Res. 2016;44(6):1376–80.
doi: 10.1177/0300060516669897
pubmed: 27789806
pmcid: 5536752
Larkin C, O’Brien D, Maheshwari D. Anaesthesia for Epilepsy surgery. BJA Educ. 2019;19(12):383.
doi: 10.1016/j.bjae.2019.08.001
pubmed: 33456862
pmcid: 7807957
Jellish WS, Edelstein S. Neuroanesthesia. Handb Clin Neurol. 2014;121:1623–33.
doi: 10.1016/B978-0-7020-4088-7.00106-1
pubmed: 24365438
Soriano SG, Martyn J. Antiepileptic-Induced Resistance to Neuromuscular blockers. Clin Pharmacokinet. 2004;43(2):71–81.
doi: 10.2165/00003088-200443020-00001
pubmed: 14748617
Sacré A, Jouret F, Manicourt D, Devuyst O. Topiramate induces type 3 renal tubular acidosis by inhibiting renal carbonic anhydrase. Nephrol Dialysis Transplantation. 2006;21(10):2995–6.
doi: 10.1093/ndt/gfl251
Stowe CD, Bolliger T, James LP, Haley TM, Griebel ML, Farrar HC III. Acute mental status changes and hyperchloremic metabolic acidosis with long-term topiramate therapy. Pharmacotherapy: J Hum Pharmacol Drug Therapy. 2000;20(1):105–9.
doi: 10.1592/phco.20.1.105.34662
Izzedine H, Launay-Vacher V, Deray G. Topiramate-induced renal tubular acidosis. Am J Med. 2004;116(4):281–2.
doi: 10.1016/j.amjmed.2003.08.021
pubmed: 14969660
Rodriguez L, Valero R, Fàbregas N. Intraoperative metabolic acidosis induced by chronic topiramate intake in neurosurgical patients. J Neurosurg Anesthesiol. 2008;20(1):67–8.
doi: 10.1097/ANA.0b013e31815613ad
pubmed: 18157030
Wilner A, Raymond K, Pollard R. Topiramate and metabolic acidosis. Epilepsia. 1999;40(6):792–5.
doi: 10.1111/j.1528-1157.1999.tb00781.x
pubmed: 10368081
Ruiz-Granados VJ, Márquez-Romero JM. Topiramate in monotherapy or in combination as a cause of metabolic acidosis in adults with epilepsy. Rev Neurol. 2015;60:159–63.
pubmed: 25670045
De Simone G, Scozzafava A, Supuran CT. Which carbonic anhydrases are targeted by the antiepileptic sulfonamides and sulfamates? Chem Biol Drug Des. 2009;74(3):317–21.
doi: 10.1111/j.1747-0285.2009.00857.x
pubmed: 19703035
Purkerson JM, Schwartz GJ. The role of carbonic anhydrases in renal physiology. Kidney Int. 2007;71(2):103–15.
doi: 10.1038/sj.ki.5002020
pubmed: 17164835
Inoue T, Kira R, Kaku Y, Ikeda K, Gondo K, Hara T. Renal tubular acidosis associated with zonisamide therapy. Epilepsia. 2000;41(12):1642–4.
doi: 10.1111/j.1499-1654.2000.001642.x
pubmed: 11114225
Garris SS, Oles KS. Impact of topiramate on serum bicarbonate concentrations in adults. Annals Pharmacotherapy. 2005;39(3):424–6.
doi: 10.1345/aph.1E437
Montenegro MA, Guerreiro MM, Scotoni AE, Guerreiro CA. Predisposition to metabolic acidosis induced by topiramate. Arq Neuropsiquiatr. 2000;58(4):1021–4.
doi: 10.1590/S0004-282X2000000600007
pubmed: 11105067
Lim BL, Kelly AM. A meta-analysis on the utility of peripheral venous blood gas analyses in exacerbations of chronic obstructive pulmonary disease in the emergency department. Eur J Emerg Medicine: Official J Eur Soc Emerg Med. 2010;17(5):246–8.
doi: 10.1097/MEJ.0b013e328335622a
Ruan Y, Chen L, She D, Chung Y, Ge L, Han L. Ketogenic diet for epilepsy: an overview of systematic review and meta-analysis. Eur J Clin Nutr. 2022;76(9):1234–44.
doi: 10.1038/s41430-021-01060-8
pubmed: 35027683
Heo G, Kim SH, Chang MJ. Effect of ketogenic diet and other dietary therapies on anti-epileptic drug concentrations in patients with epilepsy. J Clin Pharm Ther. 2017;42(6):758–64.
doi: 10.1111/jcpt.12578
pubmed: 28626875
Bjurulf B, Magnus P, Hallböök T, Strømme P. Potassium citrate and metabolic acidosis in children with epilepsy on the ketogenic diet: a prospective controlled study. Dev Med Child Neurol. 2020;62(1):57–61.
doi: 10.1111/dmcn.14393
pubmed: 31745987
Starke A, Corsenca A, Kohler T, Knubben J, Kraenzlin M, Uebelhart D, Wüthrich RP, von Rechenberg B, Müller R, Ambühl PM. Correction of metabolic acidosis with potassium citrate in renal transplant patients and its effect on bone quality. Clin J Am Soc Nephrology: CJASN. 2012;7(9):1461–72.
doi: 10.2215/CJN.01100112