Succinylcholine Apnea in an Unusual Case Posted for Dentigerous

Cyst Excision

Case Report

INTRODUCTION

Succinylcholine causes a depolarizing type ofneuromuscular block. This drug is unique in its rapid onsetand short duration. This drug has been the mainstay of theanesthesiologist’s armamentarium for the last 60 years andis still being used actively throughout the world despite itsmany disadvantages and some potentially lethal dangers.

CASE REPORT

36 years old gentlemen from West Bengal, weighing 74kgs, was posted for dentigerous cyst excision in themaxillary region. The preoperative evaluation andinvestigations were within normal limits. Patient wasplanned for general anesthesia under ASA physical status I.

Patient was induced with Inj. Propofol 140mg, Fentanyl70 mcg. Intubation was facilitated using Inj.Succinylcholine 100 mg. Subsequently Inj. Atracurium 30mg was given. The patient was maintained with sevofluranein nitrous oxide:oxygen mixture. Surgery lasted for 50minutes. At the end of the case, anesthesia was discontinuedand allowed to emerge. Oral suctioning was done guided bylaryngoscope. Patient was reversed with Inj. Neostigmine2.5 mg and Inj. Glycopyrrolate 0.4 mg. Patient had jerkymovements with inadequate muscle power and inefficientrespiratory efforts. Hypercarbia developed. It was decidedto wait for complete recovery of muscle power in theoperating room. Patient was ventilated with N2O: O2 –50:50%. After 1 hour of waiting, there was only a marginalimprovement in the muscle power and breathing. It wasdecided to send serum Pseudocholinesterase level. Reportwas obtained after 1 hour. The patient’s value was 0.3units/mL (Normal range: 5.2-13.2 units/mL). Patient was shifted

SUCCINYLCHOLINE APNEA IN AN UNUSUAL CASE POSTED FORDENTIGEROUS CYST EXCISION

R Aravindan* and Jamila***Consultant Anaesthesiologist, **Senior Resident, Apollo Hospitals, 21, Greams Lane, Off Greams Road,

Chennai 600 006, India.Correspondence to: Dr R Aravindan, *Consultant Anaesthesiologist, Apollo Hospitals, 21, Greams Lane,

Off Greams Road, Chennai 600 006, India.E-mail: arvi.r@rediffmail.com

We present a case of 36 years old male posted for dentigerous cyst excision who had delayed recovery fromthe effects of succinylcholine due to reduced serum pseudocholinesterase level.

Key words: Succinylcholine apnea, Serumpseudocholinesterase.

to intensive care unit and was ventilated with pressuresupport mode. Inj. Midazolam 1 mg was given. Five hourslater from the initial use of Succinylcholine, the patient hadregained sufficient motor function to meet extubationrequirements. Patient was subsequently weaned off to Tpiece and later extubated. After extubation, patient wasalert with no residual effects of muscle relaxant.Retrospective history from patient revealed no suchincidence in the past or to any of his family members.Patient was clearly explained about the condition he hadand was also warned about the use of succinylcholine infuture.

DISCUSSION

Succinylcholine is a potent neuromuscular blockingagent of the depolarizing type. Its effects are of shortduration, and for this reason it is widely used as a musclerelaxant during anesthesia. Since the clinical introductionof the drug in 1951, cases of prolonged apnea after its usehave been reported. The neuromuscular junction isimportant in anesthesia practice since we are often requiredto completely ablate all neuromuscular function. Thenicotine acetyl-choline (nAChr) receptor plays thedominant role in the neuromuscular junction and iscomposed of 5 subunits. Two alpha subunits must beoccupied by acetylcholine in order for Na+ ions to beallowed to pass through the protein pore causingdepolarization of the sarcolemma. Succinylcholine mimicsacetylcholine because it is essentially two acetylcholinemolecules hooked together. Succinylcholine binds to boththe alpha subunits of the receptor and causes an initialdepolarization. Succinylcholine is not rapidly cleaved likeacetylcholine and it remains in place causing the cell to

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Case Report

remain depolarized and thus paralyzed. This is referred toas Phase I block. A phase II block may occur after thesuccinylcholine overwhelms the neurmomuscular junctionby sheer numbers. After a time, the receptor itselfundergoes changes which make it less susceptible tostimulation by acetylcholine. Clinically this will presentwith a fade on train of four with a twitch monitor whichresembles the non depolarizaing muscle relaxants.Succinylcholine is hydrolyzed by pseudocholinesterasewhich is a tetrameric glycoprotein enzyme produced by theliver [2].

This patient was of ASA grade I and had no othercomorbid factors which can prolong the action ofsuccinylcholine like liver disorders or renal failure. Patientwas not hypothermic which can decrease the rate ofhydrolysis.

Only 30mg of Inj. Atracurium was given as a relaxantand neostigmine was given to antagonize its relaxationeffect only after 50 minutes. Thus the possibility of delayedrecovery from non depolarizing muscle relaxant is highlyimprobable.

The low level of serum Pseudocholinesteraseconfirmed the diagnosis of succinylcholine apnea in thispatient. The decreased level of pseudocholinesterase isunlikely due to the administration of neostigmine becausethe sample for serum pseudocholinesterase level was sent

only 1½ hours after the administration of neostigmine (t½of Neostigmine -). Low pseudocholinesterase levelsgenerally produce only modest prolongation ofsuccinylcholine’s action. Thus the delayed recovery in thispatient is likely due to decreased level ofpseudocholinesterase and not because of atypicalpseudocholinesterase where apnea may be prolonged upto48 hours.

We may find out that prolonged blocks can beencountered as a result of PChE enzyme defect whensuccinylcholine is used. This situation can either be fromcongenital as in one of our patients or due to variousreasons (pregnancy, malnutrition and sertraline use) [3]. Weanesthesiologist should be aware of serum pseudo-cholinesterase deficiency in delayed recovery when othercauses are ruled out.

REFERENCES

1. Abel M. In Depolarizing neuromuscular blockade. ClincalCases in Anesthesiology. Reed A (ed.). Philadelphia,Churchill Livingstone, 3rd ed. 2005: 117.

2. Sunew KY, et al. Effects of Neostigmine andPyridostigmine on duration of Succinylcholine action andpseudocholinesterase activity. Anesthesiology. 1978;49:188.

3. Beyazit Zencirci. Pseudocholinesterase enzymedeficiency: a case series and review of the literature.Cases Journal 2009, 2: 9148.

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