Pain Management During Labor and Delivery in a Patient with Possible Local Anesthetic Resistance: A Case Report
Aksana Aliakseyeva1, *, Dante Villarreal2, Natalia Pawlowicz3
Identifiers and Pagination:Year: 2022
E-location ID: e258964582208180
Publisher ID: e258964582208180
Article History:Received Date: 16/3/2022
Revision Received Date: 30/5/2022
Acceptance Date: 30/6/2022
Electronic publication date: 31/10/2022
Collection year: 2022
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Local anesthetic resistance is a clinical entity characterized by inadequate analgesia despite technically well-performed procedures. The exact etiology and pathogenesis of this condition are not yet fully understood.
A 36-year-old Caucasian female presented to labor and delivery for induction of labor. On admission, the patient reported failure of epidural anesthesia during the previous delivery. An epidural catheter was placed, and analgesia was reported only at high doses of local anesthetic. The patient’s maximum pain level during delivery never reached a score of 2 out of 10.
The most common causes of regional anesthetic failure are technical or placement failure, failure related to the local anesthetic itself, or localized infection. This patient appeared to have a true local anesthetic resistance, which was overcome by doubling the customary concentration of local anesthetic. Atypical responses to local anesthetics observed in the patient may be due to incomplete penetrance mutations in sodium channels since local anesthetics work through blocking nerve conduction by acting on these channels.
The most common cause of block failure is an inability to successfully access the epidural space. This may occur due to incorrect needling techniques, poor patient positioning, anatomical abnormalities, or equipment-related factors . The exact etiology and pathogenesis of true local anesthetic resistance have not yet been fully elucidated.
We report a case of a 36-year-old female who presented for induction of labor.
An epidural catheter was successfully placed on the first attempt. While sensory blockade was achieved, motor blockade was not obtained despite evidence of appropriate dermatomal distribution of sensory blockade. This clinical presentation and past medical history of this patient imply a true resistance to local anesthetics.
2. CASE PRESENTATION
A healthy 36-year-old female presented for induction of labor at Texas Health Frisco Hospital. On admission, the patient reported a failed epidural with her previous vaginal delivery 26 months ago. The last delivery was performed at another institution, and according to the provided records, sufficient analgesia was never reached with a customary dose and concentration of local anesthetic (bupivacaine 0.125% epidural block analgesia combined with fentanyl 100mcg).
The patient’s past medical history is notable for insufficient analgesia during dental procedures. Her dentist had tried various types of local anesthetics without success. She does not recall the names of the medications used, except lidocaine and bupivacaine. Her younger sister has had the same dental issues since childhood, otherwise, her family history is unremarkable. Knowing that local anesthetic resistance can be linked to scorpion bites [2-4], the patient was questioned and reported no history of such bites.
2.1. Treatment Plan
Analgesia through an epidural catheter was recommended for her delivery. We presented the patient with a detailed discussion concerning the risks and benefits of the procedure. The patient agreed that epidural analgesia would be performed; the original treatment plan to achieve proper analgesia was to increase the anesthetic concentration instead of the volume.
The patient was prepared for epidural placing. After sterile skin preparation, a skin dose of 3 mL 1% volume lidocaine was infiltrated. On insertion of a 17-gauge Tuohy needle into the skin, the patient complained of moderate pain. Test dose with 3 ml 1.5% lidocaine and epinephrine 1:200000 was negative.
The patient then received a bolus of 100mcg fentanyl, and 10 mL of 0.5% ropivacaine and noted warmth in her feet and buttocks. Of note, 0.2% Ropivacaine is customarily used for epidural bolus and infusion at our institution. It is recommended to administer a 10-20 ml bolus of ropivacaine 0.2% with intermittent 20-30 mg top-up injections or a continuous epidural infusion of ropivacaine 0.2% (6-10 ml/hr) for labor analgesia [5-7]. Anticipating difficulties with adequate analgesia, we utilized a higher (0.5%) Ropivacaine concentration from the start of the case. Thirty minutes later, the patient was given 6 mL 0.5% ropivacaine through a programmed intermittent epidural bolus pump (PIEB). The patient started complaining of excessive numbness in her legs around two hours later. Ice and light touch sensation testing showed diminished temperature and nociception perception at the T10 level, respectively. As a result, PIEB dosage of 0.5% ropivacaine was decreased to 4 mL. Two hours later, the patient’s PIEB dosage was increased to 5 mL, and a bolus of 2 mL of 0.5% ropivacaine and 100 mcg fentanyl was given due to increasing pain. In the evening, augmentation of labor with oxytocin was started, and the baby was delivered shortly thereafter with adequate pain control. Post-delivery, the patient received 800 mg of Ibuprofen PO.
2.2. Expected and Atual Outcome
The modified treatment plan of increasing the concentration of local anesthetic from the start, in conjunction with occasional bolus doses of fentanyl, resulted in the desired analgesic effect. The patient’s maximum pain level during full dilation never reached a score of 2 out of 10.
3. RESULTS AND DISCUSSION
This particular case is important to the medical world because it accentuates one of the few documented cases of local anesthetic resistance where the patient achieved appropriate analgesia. The approach used to reach proper analgesia was to double the concentration of the local anesthetic, while maintaining the same volume, compared to routine labor and delivery cases .
The transmembrane membrane segment S6 of domain IV of the Na+ channel alpha subunit is believed to be the local anesthetic receptor site. Specifically, more contemporary research has found only 2 residues on this S6 segment that greatly affected the affinity to the LA: Phe-1764 and Tyr-1771 [5, 6]. Given this information, a possible explanation could be a mutation in one or both of these residues in this S6 transmembrane segment. Increasing the dosage of the anesthetic would thus have allowed more receptors to come into contact with the anesthetic. We chose to augment the concentration, rather than volume to prevent excessive epidural spread while maximizing receptor saturation. A higher number of receptors would be able to come into contact with the anesthetic, increasing the chance of receptor activation. Thus, the treatment plan targeted the suspected receptor site mutation by attempting to saturate the receptor site and recruit more receptors .
We presented a patient with possible local anesthetic resistance, a history of multiple failures of local dental anesthetic in the past, and a family history of similar symptoms. We were able to achieve proper labor epidural analgesia in this patient after increasing the routinely received concentration of local anesthetic. Since sufficient analgesia level was achieved, presented local anesthetic resistance may be due to incomplete penetrance or genetic alterations in the sodium channel which were overcome by presumed receptor saturation.
AA: conceptualization, writing of the original draft, review, and editing. DV: conceptualization, writing of the original draft, review, and editing. NP: conceptualization, writing of the review, and editing.
LIST OF ABBREVIATIONS
|PIEB||= Programmed Intermittent Epidural Bolus Pump.|
|LA||= Local Anesthetic.|
ETHICS APPROVAL AND CONSENT TO PARTICIPATE
HUMAN AND ANIMAL RIGHTS
CONSENT FOR PUBLICATION
Written informed consent was obtained from the patient for publication of this case report.
STANDARDS OF REPORTING
CARE guidelines and methodology were followed.
AVAILABILITY OF DATA AND MATERIALS
The data used to support the findings of this study are available from the corresponding author on request [A.A], except for the patient's personal health information due to Health Insurance Portability and accountability regulations.
CONFLICT OF INTERESTS
The authors declare that they have no conflicts of interest.
|||Rae JD, Fettes PDW. Mechanisms and Management of Failed Spinal Anesthesia 2021.www.nysora.com/foundations-of-regional-anesthesia/complications/mechanisms-|
|||Murthy V, Venkata Ramana. Local anesthesia failure cases with scorpion bite history in third molar surgery- A challenge ARC J Anesthesiol 2017; 2(2): 7-10.www.arcjournals.org/pdfs/aja/v2-i2/3.pdf|
|||Panditrao M, Panditrao M, Sunilkumar V, Panditrao A. Effect of previous scorpion bite(s) on the action of intrathecal bupivacaine: A case control study. Indian J Anaesth 2013; 57(3): 236-40.
|||Panditrao M, Panditrao M, Khan MI, Yadav N. Does scorpion bite lead to development of resistance to the effect of local anaesthetics? Indian J Anaesth 2012; 56(6): 575-8.
|||Ragsdale DS, McPhee JC, Scheuer T, Catterall WA. Molecular determinants of state-dependent block of Na+ channels by local anesthetics. Science 1994; 265(5179): 1724-8.
|||Yarov-Yarovoy V, McPhee JC, Idsvoog D, Pate C, Scheuer T, Catterall WA. Role of amino acid residues in transmembrane segments IS6 and IIS6 of the Na+ channel alpha subunit in voltage-dependent gating and drug block. J Biol Chem 2002; 277(38): 35393-401.
|||Kuthiala G, Chaudhary G. Ropivacaine: A review of its pharmacology and clinical use. Indian J Anaesth 2011; 55(2): 104-10.
|||Skelly MF, Kondash S, Mazer SM, Conter EA, Bosmann HB. Properties of a local anesthetic receptor in rat brain. Life Sci 1986; 38(17): 1607-16.