Dear Editor,
Anesthetic agents can play a role in the exacerbation of multiple sclerosis (MS) and increase the risk of neurological dysfunction.[1] Ketamine reported to have neuroprotective effects due to its anti-inflammatory effects by suppression of NF-kappaB, which is involved in brain neurodegenerative process in MS and can be a preferred anesthetic agent in those patients.[2,3] We are reporting the anesthetic management of an MS patient posted for an MRI procedure under balanced intravenous anesthesia “Ketofol.”
A 45-year-old female had a history of stiffness of both lower limbs for ten years, followed by weakness of the left upper limb, facial pain, and diplopia for seven years, and severe backache for the last two months. She was diagnosed with MS, trigeminal neuralgia (right), asymmetric axonal polyradiculoneuropathy.
The patient was planned for MRI under general anesthesia after an initial failed attempt for MRI under midazolam sedation. In the MRI suite, all compatible standard American Society of Anesthesiologists monitor was attached. She was premedicated with glycopyrrolate 4 mcg/kg-wt., midazolam 0.02 mg/kg-wt., and fentanyl 2 mcg/kg-wt. She was pre-oxygenated, and anesthesia was induced with a combination of ketamine and propofol (1:2). After obtaining an adequate depth of anesthesia, airway was secured with I-Gel size 3. She was put on controlled ventilation after confirmation of adequate chest rise and minimal air leak on spontaneous ventilation. The depth of anesthesia was maintained with propofol infusion at a rate of 50 mcg/kg/min. The procedure MRI Brain and spinal cord with contrast successfully completed in 90 minutes. After completion of procedure the I-gel was removed after patient was conscious and obeying commands. She was monitored for one hour in post-procedure room and then shifted to the ward. Her neurological status was stable on follow-up after last two months.
MS is a disease of random and reversible demyelination at the central nervous system.[1] Infection, surgical intervention, trauma, emotional stress, and hyperthermia were associated with disease exacerbation, care must be taken to control these factors adequately. Inhalational and intravenous anesthetic agents reported to have no adverse effect on nerve conduction and not associated with disease progression.[1] Succinylcholine should be avoided, and non-depolarizing agents can be used when necessary, under strict monitoring.[1] We choose supraglottic airways (SGA) to secure the airway as it does not require muscle relaxation for its insertion and maintenance, unlike endotracheal tracheal intubation. The I-Gel SGA was used as it is compatible with the MRI suite.[4] We choose ketamine-based intravenous general anesthesia as it was reported to have neuroprotective effects due to anti-inflammatory effects by suppression of NF-kappaB.[2] NF-kappaB was reported to be involved in brain neurodegenerative, inflammatory diseases like MS.[3] Ketamine can have undesirable side effects like dizziness, euphoria, and dissociative symptoms, and propofol helps in mitigating it when used as a part of balance intravenous anesthesia combination “ketofol.”[5] Since propofol can cause dose-dependent hypotension, ketamine can prevent it by its sympathomimetic effect. The combination of drug ketofol have additive effects so that the dose of individual drugs can be decreased and benefits such as amnesia, analgesia, hypnosis, and hemodynamic stability can be achieved.[5]
To conclude, ketamine is a neuroprotective drug in patients with MS, and it can be safely used for procedural sedation, induction, and maintenance of general anesthesia in those patients.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initial s will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
Acknowledgment
We are thankful to Dr. Sanjeev Bhoi, Associate Professor department of Neurology, All India Institute of Medical Sciences, Bhubaneswar, for providing detail clinical information about the patient.
References
- 1.Dorotta IR, Schubert A. Multiple sclerosis and anesthetic implications. Curr Opin Anaesthesiol. 2002;15:365–70. doi: 10.1097/00001503-200206000-00015. [DOI] [PubMed] [Google Scholar]
- 2.Sakai T, Ichiyama T, Whitten CW, Giesecke AH, Lipton JM. Ketamine suppresses endotoxin-induced NF-kappaB expression. Can J Anaesth. 2000;47:1019–24. doi: 10.1007/BF03024876. [DOI] [PubMed] [Google Scholar]
- 3.Sakai T, Tomiyasu S, Ono T, Yamada H, Sumikawa K. Multiple sclerosis with severe pain and allodynia alleviated by oral ketamine. Clin J Pain. 2004;20:375–6. doi: 10.1097/00002508-200409000-00016. [DOI] [PubMed] [Google Scholar]
- 4.Taxak S, Bhardwaj M, Gopinath A. The i-gel (™)-A promising airway device for magnetic resonance imaging suite. J Anaesthesiol Clin Pharmacol. 2012;28:263–4. doi: 10.4103/0970-9185.94917. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 5.Andolfatto G, Abu-Laban RB, Zed PJ, Staniforth SM, Stackhouse S, Moadebi S, et al. Ketamine-propofol combination (ketofol) versus propofol alone for emergency department procedural sedation and analgesia: A randomized double-blind trial. Ann Emerg Med. 2012;59:504–12. doi: 10.1016/j.annemergmed.2012.01.017. [DOI] [PubMed] [Google Scholar]