Apnoea and prolonged paralysis after
succinylcholine administration is not an uncommon occurrence
in anaesthetic practice. It occurs due to inherited or
acquired deficiency of butyrylcholinesterase. Suxamethonium
(succinylcholine) is a depolarizing neuromuscular blocker used
for rapid sequence intubation in anesthesia. It acts quickly,
causing temporary paralysis, but in some individuals, a
deficiency or abnormality in the enzyme pseudocholinesterase
(also called butyrylcholinesterase) can result in prolonged
paralysis, a condition known as suxamethonium apnea.
Pseudocholinesterase deficiency can be inherited or acquired,
and patients with this condition cannot efficiently metabolize
suxamethonium, leading to delayed recovery from muscle
paralysis. The clinical presentation typically includes
prolonged apnea and muscle weakness long after the expected
recovery time, often requiring mechanical ventilation until
the effects of the drug wear off.
Suxamethonium is used to achieve quality relaxation for the
orotracheal intubation. It is considered as a safe drug but
can rarely lead to serious adverse effects, such as
hyperkalaemia, malignant hyperthermia, and prolonged apnoea.
Prolonged apnoea may occur due to pseudocholinesterase
deficiency, old age, impaired liver or renal function and
medication interactions.
Introduction
Prolonged paralysis and apnea after succinylcholine
administration is a well-recognized event in anesthetic
practice, often attributed to either an inherited or acquired
deficiency of butyrylcholinesterase [1, 2]. Sensitivity to
suxamethonium is a well-known risk factor, and pre-procedural
assessment for sensitivities is crucial in safety protocols.
Case report
A middle aged male was admitted with complaints of hoarseness
of voice. No voice fatigues. No voice breaks. No known drug
allergies. He is a known case of diabetes mellitus and
dyslipidemia on oral hypoglycemic agents and statins.
On examination, he was conscious, oriented, moderately built
and nourished. His vitals were stable. Other systemic
examinations were within normal limits. ENT examination
showed good oral resonance, larynx moves up on phonation.
There is hoarseness of voice. On neck bilateral thyrohyoid
intervals are tender and narrow. Oral cavity and oropharynx
normal. On videolaryngoscopy (VLS) - Bilobed polyp on the
middle 3rd of right vocal cord, anterior phonatory gap
present.
Lab investigation showed a Hb of 15.3 g/dl, platelet count of
2.51 lakh/mm
3 with normal coagulation parameters.
Liver and renal function tests were within normal limits. The
electrocardiogram showed a normal sinus rhythm and echo showed
mild mitral regurgitation, ther is no regional wall motion
abnormality, normal left ventricular function with ejection
fraction 62%. Airway examination showed a Mallampatti grade of
3.
He was admitted under ENT department and was posted for
elective micro laryngeal surgery plus biopsy under general
anaesthesia. In the past history he has undergone forearm
surgery under GA. He said that surgery was uneventful. On
repeated questioning, bystander said that some delay was there
after previous surgery for shifting back from OT. This history
was given by bystander after the surgery when scoline
apnoea haf already been noted.
He was premedicated with midazolam 1mg, pantoprazole
40mg, dexamethasone 16mg, glycopyrrolate 0.2mg, metoclopramide
10mg intravenously. In operation theatre, all standard ASA
monitors including 5 lead ECG with ST segment monitoring,
pulse oximetry and noninvasive blood pressure were attached.
Room air saturation was 98%. Preoxygenation with 100% oxygen
was initiated with Hudson mask at 6L/minute for 3 minutes.
Warm saline was started on a 18G cannula on the left forearm.
Then fentanyl 100 mcg was given IV. Then he was precurarized
with atracurium 5mg IV and induced with propofol 160mg IV, and
succinyl choline 100 mg was given for muscle relaxation. After
1.5 minutes, he was intubated with a 6 size MLS tube and fixed
at 22 cm. The cuff was inflated to pressure of 25 cm of
H
2O and bolus atracurium 40 mg was given. A suction
catheter of size 14 G was inserted to deflate the stomach. The
patient was mechanically ventilated with pressure
control volume guaranteed mode using closed circuit and end
tidal carbon dioxide was monitored. The ventilatory settings
were adjusted as tidal volume 625 ml, RR-15, PEEP-5cm H
2O,
FIO2-50%. Maintenance was carried out using oxygen, air,
desflurane 6%, and bolus doses of atracurium ensuring
adequate depth.
Under GA, patient was positioned and direct laryngoscopy was
done. Endoscopic resection of right vocal cord polyp excised
in toto, after infiltration with lignocaine and adrenaline.
Reinke's space was reconstructed. Internal and external
laryngeal block given. The surgical procedure was uneventful.
Post-extubation, the patient had a sudden breathing difficulty
and he developed suspected laryngospasm. Positive pressure
ventilation was continued but spontaneous breathing didn't
return. I-gel was inserted, and assisted ventilation
continued. Neuromuscular monitoring showed a prolonged
paralysis. Spontaneous respiration returned after 4 hours and
once adequate power and recovery from muscle relaxants as per
neuromuscular monitoring, he was extubated. Subsequently we
got the laboratory investigations which showed low plasma
cholinesterase activity. He remained haemodynamically stable
throughout and was discharged in good condition the next day.
Discussion
Management of Scoline Apnea
Immediate Management
1. Supportivecare
The patient is kept unconscious with anaesthetic agents and
placed on mechanical ventilation until muscle function
returns.
2. Neuromuscular Monitoring
A nerve stimulator (Train of Four) is used to assess
recovery. Full return of muscle strength is confirmed by
four strong twitches without fade.
3. Allow Natural Recovery
No reversal agents are used. Recovery is monitored until the
patient can breathe independently, follow commands, grip
firmly, and lift their head.
4. Fresh Frozen Plasma (FFP)
In severe cases, FFP can be given to provide the missing
enzyme. However, it is not routinely used due to risks
associated with blood transfusion.
Special Considerations
● Pseudocholinesterase Deficiency
This inherited enzyme deficiency is the most common cause of
prolonged scoline apnea.
● Genetic Testing
Patients and their families should be offered genetic
testing to identify pseudocholinesterase variants.
Recovery and Follow-Up