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 Table of Contents  
CASE REPORT
Year : 2022  |  Volume : 1  |  Issue : 2  |  Page : 74-76

Demystifying a hassle in obstetric anaesthesia: A case report


Department of Anaesthesia and Intensive Care, Government Medical College and Hospital, Chandigarh, India

Date of Submission21-Apr-2022
Date of Decision10-Jun-2022
Date of Acceptance11-Aug-2022
Date of Web Publication02-Dec-2022

Correspondence Address:
Dr. Sahil Garg
Department of Anaesthesia and Intensive Care, Government Medical College and Hospital, Sector 32, Chandigarh - 160 030
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jica.jica_13_22

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  Abstract 

We report a case of primigravida posted for emergency lower segment cesarean section (LSCS). She had to be administered general anesthesia due to failure of the spinal blockade. While the intraoperative period remained uneventful, the patient could not be extubated after the procedure due to poor respiratory efforts and motor power. She was shifted to the intensive care unit where, after several hours, she could be extubated. On follow-up and further workup, the pseudocholinesterase enzyme was found to be deficient in the patient's blood reports. This case report aims to highlight the importance of considering the deficiency of pseudocholinesterase while managing obstetric patients while suggesting deliberations and relevant management.

Keywords: Delayed awakening, dilemma, obstetric anesthesia


How to cite this article:
Upadhyay P, Garg S. Demystifying a hassle in obstetric anaesthesia: A case report. J Ind Coll Anesth 2022;1:74-6

How to cite this URL:
Upadhyay P, Garg S. Demystifying a hassle in obstetric anaesthesia: A case report. J Ind Coll Anesth [serial online] 2022 [cited 2023 Feb 4];1:74-6. Available from: https://www.jicajournal.in//text.asp?2022/1/2/74/362606


  Introduction Top


Anesthesiologists have come a long way in managing obstetric patients. Obstetric anesthesia is both rewarding and challenging, and obstetric patients recover well with critical care.[1] Cesarean sections are now widely performed as an emergency and elective procedure under spinal anesthesia. General anesthesia (GA) is being used less often and for specific indications. We discuss a case of failed spinal anesthesia followed by delayed awakening from GA in a patient undergoing lower segment cesarean section (LSCS) while suggesting deliberations and strategies of management.


  Case Report Top


A 25-year-old female presented as primigravida at 37 weeks and 1 day of gestation in view of beech in labor with short stature. She had a chief complaint of intermittent pain abdomen for 3 days which increased in frequency and intensity in the last 4 h. The patient perceived adequate fetal movements. The obstetric history was uneventful.

On general physical examination, no abnormality was detected and vitals were within normal limits. On per-abdomen examination, the uterus was around 36 weeks with breech. Routine baseline investigations were within normal limits [Table 1]. The patient was taken for emergency LSCS in view of breech in labor.
Table 1: Preoperative investigations

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The patient was taken on the operation theater (OT) table after nil-per-oral confirmation and brief history and examination. Routine monitors were attached, and two wide bore intravenous lines were secured. Under absolute aseptic precautions, subarachnoid block (SAB) was administered with 26-gauge Quincke needle with 12 mg of heavy bupivacaine after confirming good backflow of cerebrospinal fluid (CSF) in the sitting position in L4–L5 interspace. The patient was made supine; however, no effect of spinal anesthesia was evident for 15 min. SAB was repeated with 10 mg heavy bupivacaine by senior resident under due care. Again, there was a failure of spinal anesthesia with no effect observed for 15 min. The decision to proceed with GA was taken. Rapid sequence induction was performed with propofol and succinylcholine and maintained with inhalation 60:40 nitrous oxide: oxygen with isoflurane to maintain end-tidal anesthetic concentration of 1.0. The patient showed wearing off of succinylcholine at 8 min with curare notch, tachycardia, and spontaneous tidal volume (TV) of 30–40 ml. Atracurium 0.5 mg/kg was administered. Oxytocin, fentanyl, paracetamol, and ondansetron were administered intraoperatively as indicated. The patient's surgery went on for 50 min. There was no need to repeat the injection atracurium during the intraoperative period.

On completion, inhalational agents were switched off. The patient started to take spontaneous breaths and reversed with 0.05 mg/kg neostigmine and 10 μg/kg glycopyrrolate. However, the patient could not be completely reversed. Arterial blood gas analysis was within normal limits. The patient had inadequate respiratory efforts – her spontaneous TV ranging between 30 and 70 ml and breaths being shallow and irregular. The patient was able to move hands, feet, and eyelids in twitching gestures on being called. In view of prolonged recovery from neuromuscular blockade, she was monitored in the OT. The patient was euthermic, non-acidotic, and wincing to pinprick in lower limbs. She was then shifted to the intensive care unit (ICU) for postoperative monitoring and care. She was ventilated on pressure support ventilation with inspired oxygen concentration of 40%, positive end-expiratory pressure of 4, and pressure support of 10. Gradually, the support was tapered down in accordance with ventilatory efforts. She was extubated after 6 h of shifting uneventfully. Oxygen therapy was tapered off over 12 h, and then, she was shifted to the gynecology ward.

The patient was followed up to investigate the failure of spinal anesthesia and delayed emergence from GA. The follow-up was centered on evaluating the possibility of high spinal anesthesia that could have led to delayed recovery although unusual to occur this late. She was enquired about any similar episode in relatives and scorpion/snakebite which was absent. Local infiltration (LA) test was performed, and it demonstrated an area of local numbness where LA was infiltrated.

Second, the possibility of undiagnosed hypothyroidism and pseudocholinesterase deficiency was looked for. Thyroid profile was within normal range; however, Plasma cholinesterase level was 1439 U/l against a normal range of 5100–11,700 U/l [Table 2].
Table 2: Investigations in follow-up of the patient

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  Discussion Top


The failure of the spinal anesthesia could be patient-related (history of scorpion bite), operator-related (inadequate dose, inappropriate positioning, etc.), technique-related (misplaced injection, pseudopuncture, etc.), or equipment-related (reduced drug potency, resistance, etc.).[2] Failed SAB was likely due to a defective drug because, despite proper technique and adequate backflow of CSF, the drug did not elicit any effect. Besides, the patient was able to move her feet after the reversal was administered.

As for delayed awakening, the case appears to be of plasma cholinesterase deficiency also known as pseudocholinesterase or butyrylcholinesterase deficiency. This condition results in the prolongation of the effects of the drugs metabolized by the enzyme – succinylcholine, and mivacurium. It has been observed that homozygosity of a genetic variant was responsible for the most pronounced prolongation of neuromuscular blockade. It has a male preponderance with the highest prevalence in Caucasian males, the Persian Jewish population, and a few Alaskan tribes.[3] The incidence of homozygosity is reported to be 1 per 2000–5000 people and 1 per 500 for heterozygosity for an abnormal pseudocholinesterase enzyme.[4],[5],[6] In India, the Arya Vysya community has the highest prevalence with a mutation incidence rate of 2%–4%.[7] Hence, it is a rare but potentially fatal underlying condition. Such patients may be rendered paralyzed for several hours after an intubating dose of suxamethonium necessitating postoperative mechanical ventilation. Modest prolongation is observed with other more common factors such as elderly patients, obstetric patients, severe liver disease, burns, renal failure, echothiophate eye drops, oral contraceptive pills, and certain drugs.[8] The enzyme could also be atypical and thus functionally deficient. In these cases, diagnosis is made on suspicion, when the patient demonstrates an unexpectedly prolonged response to suxamethonium.

The prolongation of succinylcholine's action is by 2–4 min in obstetric patients due to decrease in the production of the pseudocholinesterase enzyme during pregnancy and the postpartum period. This becomes a major airway consideration due to more frequent difficulties in securing the airway and quicker desaturation.[9] As in this case, some degree of recovery from succinylcholine-induced was observed before administration of a nondepolarizing neuromuscular blocking agent (NMBA), as administration of a nondepolarizing NMBA before observed recovery from succinylcholine would confound with management.

While coming to manage such cases, the causes for prolonged block other than pseudocholinesterase deficiency should be ruled out, including opioid-induced central respiratory depression, hypothermia, and electrolyte disorders. Neuromuscular monitoring should be performed and a train-of-four fade is indicative of Phase II block that is likely to occur in these patients while lack of fade may indicate resolution of Phase II block, but the degree of recovery from Phase I block cannot be assessed without a baseline, i.e., preneuromuscular block twitch. The subjective/qualitative monitoring with a peripheral nerve stimulator is warranted if quantitative monitoring is not available. Neostigmine-induced prolonged neuromuscular blockade in a patient with atypical pseudocholinesterase can occur, and hence, reversal with neostigmine should not be attempted.[10] The patient should be sedated and mechanically ventilated until the full return of muscle strength as determined by quantitative monitoring if available. Meanwhile, optimal sedation should be ensured to decrease the risk of awareness.[5]

In a follow-up in such patients, certain investigations need to be done to measure the level and activity of butyrylcholinesterase. Dibucaine number indicates the percent of inhibition of the enzyme under standardized test conditions. Dibucaine inhibition is a phenotype testing hence, not affected by anesthetic exposure. A value of 70%–80% indicates a normal enzyme, whereas 20%–30% indicates a homozygous atypical enzyme. The blood sample for these tests should be drawn after the patient has recovered full muscle strength since the enzyme activity results can vary depending on anesthetic exposure.

Management for those previously diagnosed with pseudocholinesterase deficiency includes the avoidance of depolarizing neuromuscular blocker succinylcholine and the nondepolarizing muscular blocker mivacurium. Other nondepolarizing neuromuscular blockers such as atracurium, rocuronium, and vecuronium are safe for use in future anesthetics.[11] Ventilator backup, however, should be preferred. Limitations of this case discussion were that neuromuscular monitoring was not available, and the dibucaine number test was not investigated due to nonavailability in the hospital.


  Conclusion Top


We strongly recommend considering pseudocholinesterase deficiency in obstetric patients before proceeding with GA, quantitative neuromuscular monitoring for all patients receiving neuromuscular block, and documentation of pseudocholinesterase deficiency in file and discharge card of the patient and their counseling for future incidences.

Although rare, it is potentially life-threatening. Obstetric patients demand particularly high-suspicion in lack of time for a detailed preanesthetic checkup and the increased prevalence of this condition in this group.

Informed consent

The patient's informed written consent for publication was obtained.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for images and other clinical information to be reported in the journal. The patient understands that names and initials will not be published, and due efforts will be made to conceal patient identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Joseph CM, Bhatia G, Abraham V, Dhar T. Obstetric admissions to tertiary level Intensive Care Unit – Prevalence, clinical characteristics and outcomes. Indian J Anaesth 2018;62:940-4.  Back to cited text no. 1
  [Full text]  
2.
Parikh KS, Seetharamaiah S. Approach to failed spinal anaesthesia for caesarean section. Indian J Anaesth 2018;62:691-7.  Back to cited text no. 2
[PUBMED]  [Full text]  
3.
Lurati AR. Organophosphate exposure with pseudocholinesterase deficiency. Workplace Health Saf 2013;61:243-5.  Back to cited text no. 3
    
4.
Robles A, Michael M, McCallum R. Pseudocholinesterase deficiency: What the proceduralist needs to know. Am J Med Sci 2019;357:263-7.  Back to cited text no. 4
    
5.
Thomsen JL, Nielsen CV, Eskildsen KZ, Demant MN, Gätke MR. Awareness during emergence from anaesthesia: Significance of neuromuscular monitoring in patients with butyrylcholinesterase deficiency. Br J Anaesth 2015;115 Suppl 1:i78-88.  Back to cited text no. 5
    
6.
Zencirci B. Pseudocholinesterase enzyme deficiency: A case series and review of the literature. Cases J 2009;2:9148.  Back to cited text no. 6
    
7.
Ramaiah M, Ramakrishna P. Pseudocholinesterase deficiency in an Indian community. J Pharm Pract Community Med 2017;3:27-30.  Back to cited text no. 7
    
8.
Andersson ML, Møller AM, Wildgaard K. Butyrylcholinesterase deficiency and its clinical importance in anaesthesia: A systematic review. Anaesthesia 2019;74:518-28.  Back to cited text no. 8
    
9.
Mushambi MC, Kinsella SM, Popat M, Swales H, Ramaswamy KK, Winton AL, et al. Obstetric Anaesthetists' Association and Difficult Airway Society guidelines for the management of difficult and failed tracheal intubation in obstetrics. Anaesthesia 2015;70:1286-306.  Back to cited text no. 9
    
10.
Ramirez JG, Sprung J, Keegan MT, Hall BA, Bourke DL. Neostigmine-induced prolonged neuromuscular blockade in a patient with atypical pseudocholinesterase. J Clin Anesth 2005;17:221-4.  Back to cited text no. 10
    
11.
Lee S, Han JW, Kim ES. Butyrylcholinesterase deficiency identified by preoperative patient interview. Korean J Anesthesiol 2013;65:S1-3.  Back to cited text no. 11
    



 
 
    Tables

  [Table 1], [Table 2]



 

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