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.

1. Succinylcholine Apnea in an Unusual Case Posted for Dentigerous
Cyst Excision

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. 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.

4. Apollohospitals:http://www.apollohospitals.com/
Twitter:https://twitter.com/HospitalsApollo
Youtube:http://www.youtube.com/apollohospitalsindia
Facebook:http://www.facebook.com/TheApolloHospitals
Slideshare:http://www.slideshare.net/Apollo_Hospitals
Linkedin:http://www.linkedin.com/company/apollo-hospitals
Blog:Blog:http://www.letstalkhealth.in/