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Succinylcholine Apnea in an Unusual Case Posted for Dentigerous Cyst Excision

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

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Succinylcholine Apnea in an Unusual Case Posted for Dentigerous Cyst Excision

  1. 1. Succinylcholine Apnea in an Unusual Case Posted for Dentigerous Cyst Excision
  2. 2. Case Report INTRODUCTION Succinylcholine causes a depolarizing type of neuromuscular block. This drug is unique in its rapid onset and short duration. This drug has been the mainstay of the anesthesiologist’s armamentarium for the last 60 years and is still being used actively throughout the world despite its many disadvantages and some potentially lethal dangers. CASE REPORT 36 years old gentlemen from West Bengal, weighing 74 kgs, was posted for dentigerous cyst excision in the maxillary region. The preoperative evaluation and investigations were within normal limits. Patient was planned for general anesthesia underASAphysical status I. Patient was induced with Inj. Propofol 140mg, Fentanyl 70 mcg. Intubation was facilitated using Inj. Succinylcholine 100 mg. Subsequently Inj. Atracurium 30 mg was given.The patient was maintained with sevoflurane in nitrous oxide:oxygen mixture. Surgery lasted for 50 minutes.At the end of the case, anesthesia was discontinued and allowed to emerge. Oral suctioning was done guided by laryngoscope. Patient was reversed with Inj. Neostigmine 2.5 mg and Inj. Glycopyrrolate 0.4 mg. Patient had jerky movements with inadequate muscle power and inefficient respiratory efforts. Hypercarbia developed. It was decided to wait for complete recovery of muscle power in the operating room. Patient was ventilated with N2O: O2 – 50:50%. After 1 hour of waiting, there was only a marginal improvement in the muscle power and breathing. It was decided to send serum Pseudocholinesterase level. Report was obtained after 1 hour. The patient’s value was 0.3units/ mL (Normal range: 5.2-13.2 units/mL). Patient was shifted SUCCINYLCHOLINE APNEAIN AN UNUSUAL CASE POSTED FOR DENTIGEROUS 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 from the effects of succinylcholine due to reduced serum pseudocholinesterase level. Key words: Succinylcholine apnea, Serumpseudocholinesterase. to intensive care unit and was ventilated with pressure support mode. Inj. Midazolam 1 mg was given. Five hours later from the initial use of Succinylcholine, the patient had regained sufficient motor function to meet extubation requirements. Patient was subsequently weaned off to T piece and later extubated. After extubation, patient was alert with no residual effects of muscle relaxant. Retrospective history from patient revealed no such incidence in the past or to any of his family members. Patient was clearly explained about the condition he had and was also warned about the use of succinylcholine in future. DISCUSSION Succinylcholine is a potent neuromuscular blocking agent of the depolarizing type. Its effects are of short duration, and for this reason it is widely used as a muscle relaxant during anesthesia. Since the clinical introduction of the drug in 1951, cases of prolonged apnea after its use have been reported. The neuromuscular junction is important in anesthesia practice since we are often required to completely ablate all neuromuscular function. The nicotine acetyl-choline (nAChr) receptor plays the dominant role in the neuromuscular junction and is composed of 5 subunits. Two alpha subunits must be occupied by acetylcholine in order for Na+ ions to be allowed to pass through the protein pore causing depolarization of the sarcolemma. Succinylcholine mimics acetylcholine because it is essentially two acetylcholine molecules hooked together. Succinylcholine binds to both the alpha subunits of the receptor and causes an initial depolarization. Succinylcholine is not rapidly cleaved like acetylcholine and it remains in place causing the cell to 145 Apollo Medicine, Vol. 8, No. 2, June 2011
  3. 3. Apollo Medicine, Vol. 8, No. 2, June 2011 146 Case Report remain depolarized and thus paralyzed. This is referred to as Phase I block. A phase II block may occur after the succinylcholine overwhelms the neurmomuscular junction by sheer numbers. After a time, the receptor itself undergoes changes which make it less susceptible to stimulation by acetylcholine. Clinically this will present with a fade on train of four with a twitch monitor which resembles the non depolarizaing muscle relaxants. Succinylcholine is hydrolyzed by pseudocholinesterase which is a tetrameric glycoprotein enzyme produced by the liver [2]. This patient was of ASA grade I and had no other comorbid factors which can prolong the action of succinylcholine like liver disorders or renal failure. Patient was not hypothermic which can decrease the rate of hydrolysis. Only 30mg of Inj. Atracurium was given as a relaxant and neostigmine was given to antagonize its relaxation effect only after 50 minutes. Thus the possibility of delayed recovery from non depolarizing muscle relaxant is highly improbable. The low level of serum Pseudocholinesterase confirmed the diagnosis of succinylcholine apnea in this patient. The decreased level of pseudocholinesterase is unlikely due to the administration of neostigmine because the sample for serum pseudocholinesterase level was sent only 1½ hours after the administration of neostigmine (t½ of Neostigmine -). Low pseudocholinesterase levels generally produce only modest prolongation of succinylcholine’s action. Thus the delayed recovery in this patient is likely due to decreased level of pseudocholinesterase and not because of atypical pseudocholinesterase where apnea may be prolonged upto 48 hours. We may find out that prolonged blocks can be encountered as a result of PChE enzyme defect when succinylcholine is used. This situation can either be from congenital as in one of our patients or due to various reasons (pregnancy, malnutrition and sertraline use) [3].We anesthesiologist should be aware of serum pseudo- cholinesterase deficiency in delayed recovery when other causes are ruled out. REFERENCES 1. Abel M. In Depolarizing neuromuscular blockade. Clincal Cases in Anesthesiology. Reed A (ed.). Philadelphia, Churchill Livingstone, 3rd ed. 2005: 117. 2. Sunew KY, et al. Effects of Neostigmine and Pyridostigmine on duration of Succinylcholine action and pseudocholinesterase activity. Anesthesiology. 1978; 49:188. 3. Beyazit Zencirci. Pseudocholinesterase enzyme deficiency: a case series and review of the literature. Cases Journal 2009, 2: 9148.
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