Pseudocholinesterase Deficiency Considerations: A Case Study

Abstract

Pseudocholinesterase deficiency, sometimes called butyrylcholinesterase deficiency, is a rare disorder in which the neuromuscular blocking drugs succinylcholine and mivacurium cannot be metabolized properly in the blood plasma. This disorder can either be acquired as a result of certain comorbidities or it can be inherited genetically. Anesthesia providers must understand the pathophysiology of pseudocholinesterase deficiency and be prepared to safely and effectively manage patients who show signs and symptoms consistent with the disorder after the use of the indicated neuromuscular blocking drugs. This article summarizes the pharmacologic and physiologic data relevant to understanding the basic pathophysiology associated with pseudocholinesterase deficiency and illustrates a case study of a young woman suspected of having the disorder after a prolonged delay in emergence from general anesthesia.

CASE STUDY

A 33-year-old woman of Turkish descent (height 160 cm; weight 45.6 kg; body mass index 17.8 kg/m²) presented for treatment of mandibular retrognathism and apertognathia by surgical bilateral split osteotomy and LeFort I osteotomy under general anesthesia. The patient's medical history included a remote history of mild intermittent asthma and gastroesophageal reflux disease, and she reported having no symptoms and no longer requiring any medications. The patient reported allergies to azithromycin (swelling) and prednisone (exanthem). She denied any previous surgeries and general anesthetics.

On the day of surgery, the patient confirmed her appropriate NPO status and consented to orthognathic surgery and general anesthesia. While in the preoperative holding area, the patient's baseline vital signs were recorded, a 20-gauge intravenous (IV) was inserted into her left antecubital vein, a continuous IV drip of 0.9% sodium chloride was started, and IV midazolam (2 mg) was administered for anxiolysis. The patient was positioned on the operating table in a supine position after transport into the operating room, and standard monitors were applied, including a noninvasive blood pressure cuff, pulse oximeter, capnography, volatile agent analysis, 5-lead electrocardiogram, and axial temperature probe. The patient was then preoxygenated via face mask until her end-tidal oxygen level was greater than 90%. General anesthesia was induced with fentanyl (50 μg), propofol (150 mg), a defasciculating dose of rocuronium (5 mg), followed by succinylcholine (SCh; 100 mg). An atraumatic nasotracheal intubation was performed with a 6.5-mm nasal RAE Parker Flex-Tip tube placed through the left naris using a Macintosh size 3 blade under direct laryngoscopy. Proper nasotracheal tube placement was confirmed with equal bilateral breath sounds upon chest auscultation. The tube was secured with tape, the patient's closed eyes were covered with adhesive dressing (Tegaderm), and the patient's head was wrapped in a surgical towel for surgery. The ventilator was set to volume control parameters under continuous mandatory ventilation with tidal volumes of 400 mL, a respiratory rate of 12 bpm, and positive-end expiratory pressure of 5 cm/H₂O. General anesthesia was maintained with separate continuous infusions of propofol (300 μg/kg/min) and remifentanil (0.05–0.1 μg/kg/min). Fresh gas flows using a nitrous oxide/oxygen mix (50/50%; 2 L/min total) were administered throughout the procedure. After the patient was stabilized, an indwelling catheter was placed to monitor urine output. The patient was covered with a forced-air warming device and appropriately draped for surgery. Ampicillin-sulbactam sodium (3 g) and dexamethasone (8 mg) were administered intravenously. The operating table was then turned 90° to the anesthesia machine, and the surgical team began the procedure.

Induction of general anesthesia and draping of the patient were completed at ∼8:45 am, and the subsequent bilateral split osteotomy and LeFort surgical procedures were successfully completed in ∼4.5 hours. During the down-fracture of the maxilla, esmolol, metoprolol, and desflurane were all titrated to effect to establish intentional hypotensive anesthesia with a target mean arterial pressure of 55–60 mm Hg. At 12:45 pm, propofol and remifentanil infusions were completely discontinued. Because of their relatively short context-sensitive half-times, it was expected that the patient should emerge from general anesthesia at ∼1:15 pm, coincidental with the estimated end of surgery.^1,2 However, when the predicted emergence time arrived, the patient was still completely unresponsive to painful stimuli and not breathing spontaneously despite being relatively normocarbic and receiving no other opioids aside from the initial fentanyl bolus and remifentanil infusion. A cognitive aid was consulted, and a delayed emergence algorithm was followed. Confirmation was made that all anesthetics, both IV and inhalational, had been appropriately discontinued. Reversal of fentanyl and midazolam was considered; however, no reversal medications were given because of the prolonged time following the administration of either drug (>270 minutes) and confirmation of the patient's pupillary responses (PERRLA: pupils equal, round, and reactive to light and accommodation). Throughout the entire perioperative period, the patient never became hypoxic (SpO₂ ∼98–100%), hypercarbic (end-tidal CO₂ ∼29–36 mm Hg), hypothermic (temperature ∼36.1–37.9°C), or hypoglycemic (postoperative blood glucose 141 mg/dL). The possibility of acquired neurological defects was considered; however, because of the lack of observable focal deficits, such as anisocoria, no neurologic imaging was ordered at that time.³

At 2:00 pm, the patient had still not emerged from general anesthesia as expected. The only nondepolarizing neuromuscular blocking drug given was rocuronium at a minimal 5 mg defasciculating dose more than 5 hours earlier. A peripheral nerve monitor was placed over the ulnar nerve to assess the patient's neuromuscular status, and a train-of-four stimulus at 2 Hz was delivered. The patient displayed a characteristic sequential “fade” in the train-of-four response, indicating residual neuromuscular blockade consistent with a phase II block, which is common in patients with altered pseudocholinesterase (PChE) activity (Figure 1).⁴ Upon establishing the potential diagnosis of PChE deficiency, the anesthesia attending asked the patient to “blink your eyes” if she could hear his voice and respond to his command. The patient slowly blinked her eyes in response, although she was still intubated and not responsive to physical stimulation. To manage possible intraoperative awareness, the patient was immediately given IV midazolam (2 mg). The patient was then transferred to the postanesthesia care unit with a transport monitor while ventilation was provided with a manual bag-valve-mask and oxygen (15 L). Upon arrival to the postanesthesia care unit, the patient's nasotracheal tube was connected to a ventilator in synchronized intermittent mandatory ventilation mode. At approximately 4:15 pm, a full 7.5 hours (450 minutes) after induction of general anesthesia, the patient was able to meet all extubation criteria as confirmed by the attending anesthesiologist. The patient denied any recollection of perioperative events during an extensive postoperative interrogation.

Figure 1.

Comparison of depolarizing and nondepolarizing blocks.

PHYSIOLOGY OF THE NEUROMUSCULAR JUNCTION

The neuromuscular junction is the synapse, or site of interaction, between a somatic neuron and skeletal muscle that is composed of the nerve terminal, the synaptic cleft, and the motor end plate (Figure 2A and B).⁵ When a somatic neuron depolarizes, it releases approximately 60,000 to 100,000 acetylcholine (ACh) molecules from the presynaptic nerve terminal into the synaptic cleft.⁶ The ACh molecules transverse the ∼50-nm distance of the synaptic cleft to engage the muscle-type or nicotinic type-1 ACh receptors (N₁AChRs) located on the motor end plate. When 2 ACh molecules engage the N₁AChRs within the folds of the motor end plate, a conformational change of the receptor protein structure occurs. This results in the opening of a Na⁺ ion channel within the receptor structure, permitting the influx of Na⁺ ions into the sarcoplasm of the skeletal muscle cell, raising the transmembrane potential, and thus initiating the muscle cell depolarization. This leads to contraction of the actin-myosin complexes in the myofibrils, causing muscle contraction.⁵ After the muscle cell has depolarized, the Na⁺ channels close and are temporarily inactivated until the resting membrane potential of the cell is reestablished. Reactivation occurs quickly (within 15 ms) as the enzyme acetylcholinesterase (AChE), which is located within the synaptic cleft, rapidly metabolizes ACh into choline and acetate.^5,7 Any ACh that manages to diffuse away from the synaptic cleft is metabolized in the blood plasma by the enzyme butyrylcholinesterase (BChE).⁶ In the published literature and clinical nomenclature, BChE is commonly referred to as pseudocholinesterase or plasma cholinesterase. Because the term pseudocholinesterase (PChE) is most commonly used in the United States, it will be used in place of BChE in this article. PChE is also responsible for the metabolism of several ester-based local anesthetic and neuromuscular blocking drugs, such as chloroprocaine, cocaine, tetracaine, SCh, and mivacurium, by catalyzing the hydrolysis of choline esters.⁸

Figure 2.

(A) Neuromuscular junction. (B) Muscle-type nicotinic acetylcholine receptor (N₁AChR).

PHARMACOLOGY OF NEUROMUSCULAR BLOCKERS

Neuromuscular blocking drugs are commonly administered to patients under general anesthesia to optimize intubating conditions or to achieve skeletal muscle relaxation for surgical manipulation of tissues. Neuromuscular blocking drugs produce skeletal muscle paralysis by inhibiting the normal activity of nerve impulses upon arrival to the neuromuscular junction.⁷ Neuromuscular blocking drugs can be divided into 2 general categories: depolarizing agents and nondepolarizing agents. Depolarizing agents mimic the action of ACh at the N₁AChRs in the neuromuscular junction, causing a prolonged depolarization of the motor end plate, as evident by the initial muscular contraction or fasciculations. Nondepolarizing agents antagonize the actions of ACh at the neuromuscular junction in a classic competitive manner, preventing depolarization of the motor end plate. The main depolarizing agent in clinical use today is SCh, while the use of mivacurium has fluctuated. There are numerous nondepolarizing agents that can be divided into 3 categories based on clinical duration: long-, intermediate-, and short-acting drugs (Table 1).

Table 1.

Classification of Neuromuscular Blocking Drugs

Depolarizing neuromuscular blocking drugs

Short acting

Succinylcholine

Nondepolarizing neuromuscular blocking drugs

Short acting

Mivacurium

Intermediate acting

Rocuronium

Vecuronium

Atracurium

Cisatracurium

Long acting

Pancuronium

SCh is essentially 2 conjoined ACh molecules (Figure 3), and because of its molecular structure, SCh readily engages N₁AChRs. However, unlike ACh, SCh is not metabolized by AChE and causes prolonged depolarization of the motor endplate for approximately 5–10 minutes.⁷ Neuromuscular blockade is terminated once the SCh molecule eventually disengages from the N₁AChR and diffuses back into the neuromuscular junction, then subsequently into the extracellular fluid. SCh is eventually metabolized by PChE in the extracellular fluid and the blood plasma. Normal PChE is a glycoprotein composed of 4 identical subunits and is encoded by the gene E₁^u found on chromosome 3.⁹ Several abnormal variants of PChE exist and will be discussed in detail hereafter. Amino acid substitutions into the E₁^u gene cause PChE to have a decreased affinity for SCh, prolonging the normal metabolism of the depolarizing neuromuscular blocking drugs. Patients who have altered PChE will eventually clear SCh from the blood plasma via nonspecific plasma esterases.⁹

Figure 3.  .

Molecular structures of acetylcholine and succinylcholine.

Mivacurium, a short-acting nondepolarizing benzylisoquinolinium neuromuscular blocker, was developed as an alternative to SCh. However, it was removed from the drug market in the United States in 2006. While available in most countries, mivacurium was only reintroduced to the United States in December 2016. The normal duration of muscle blockade by mivacurium is approximately 15–20 minutes.⁴ Like SCh, mivacurium is metabolized by PChE and should not be used in patients with known PChE deficiency.

Disadvantages of SCh

SCh has been the gold standard of care for inducing skeletal muscle relaxation for ideal intubating conditions since the 1950s.¹⁰ However, SCh has many adverse side effects (some potentially life threatening) that must be considered before selecting it as a neuromuscular blocker for any anesthetic.

Administration of SCh causes a desirable phase I block, in which a prolonged depolarization of the motor endplate relaxes all skeletal muscles for approximately 5–10 minutes. The typical weight-based dosing of SCh required to accomplish a phase I block is between 1 and 1.5 mg/kg.⁷ When subsequent doses of SCh are administered immediately after the first, or if the initial dose exceeds 3–5 mg/kg, then a phase II block may occur. A phase II block, sometimes referred to as a desensitization blockade, indicates that the motor endplate has repolarized but is still not fully reactive when engaged by ACh.⁷ Phase II blocks last longer than phase I blocks and resemble a nondepolarizing neuromuscular blockade with fade during tetanic stimulation.⁷

The onset of muscle relaxation after SCh administration is typically manifest by the observance of fasciculations, which are unsynchronized contractions of skeletal muscle. The physiologic cause of fasciculations is most likely due to the action of SCh on prejunctional nicotinic receptors near the neuromuscular junction.¹¹ Fasciculations may result in postoperative myalgias of the back, neck, chest, and abdomen. Often, patients who have experienced fasciculations complain of postoperative pharyngitis, a morbidity of SCh administration that is commonly blamed on tracheal intubation.⁷

Because of its close structural resemblance to ACh, SCh has been associated with muscarinic stimulation of the myocardium resulting in arrhythmias, including acute bradycardia, sinus arrest, and atrioventricular nodal block with junctional rhythm.¹² This is especially common when SCh is used in pediatric and special needs populations. The potential muscarinic stimulation associated with SCh administration can be partially mitigated by the concurrent administration or preadministration of a muscarinic anticholinergic agent such as atropine.

SCh has the potential to cause life-threatening hyperkalemia in patients with burns, crush injuries, spinal cord injury, and congenital muscle diseases such as Duchenne's muscular dystrophy. These types of conditions result in the proliferation of immature extrajunctional N₁AChRs, which flood the blood plasma with K⁺ when stimulated. Normally, serum K⁺ levels increase by approximately 0.5 mEq/L after SCh administration. In patients with these comorbidities, serum K⁺ may rise to upward of 10 mEq/L (normally 3.5–4.5 mEq/L) after SCh administration, which may result in sudden cardiac arrest.^7,12

Complications of SCh with little-to-no clinical relevance include increases in intragastric, intraocular, and intracranial pressures.¹² Other less common complications associated with SCh administration include malignant hyperthermia, anaphylaxis, and myoglobinuria.

Pathophysiology of PChE Deficiency

The natural physiologic purpose of PChE is unknown; however, it is thought that it may be protective against AChE inhibitors and inhaled poisons.¹³ Clinically, PChE quickly degrades the depolarizing neuromuscular blocker SCh and the rapid-acting nondepolarizing neuromuscular blocker mivacurium. PChE deficiency is either a genetic or acquired disorder in which the body cannot effectively metabolize choline ester agents such as SCh and mivacurium.

When SCh is injected into the bloodstream, normally 90% of the drug is metabolized within 1 minute by PChE, leaving 10% free to perform its action within the neuromuscular junction.¹⁰ Individuals who have structurally ineffective or insufficient quantities of PChE will have higher amounts of active SCh circulating for longer amounts of time. Because PChE is synthesized in the liver, acquired PChE deficiency is often found in people with hepatic disease. Other comorbidities that can produce PChE deficiency include malnutrition, cardiac disease, renal disease, cancer, large burns, and pregnancy.¹⁰ Residual neuromuscular blockade resulting from acquired PChE deficiency typically lasts less than 1 hour.¹²

Chromosome 3q26 is the location of all mutations of the PChE gene. PChE deficiency is an autosomal recessive trait that affects approximately 1 in 2000 to 5000 individuals.¹⁰ A high incidence of PChE deficiency is found in people of Jewish-Persian, Turkish, Arya Vysya Indian, and native Alaskan descent.^2,10,14,15 To date, 5 alleles have been identified that code for PChE: usual, atypical, fluoride resistant, K variant, and silent.^14,16 Homozygous usual or normal alleles are possessed by 96% of the population, with just 4% possessing at least 1 variant allele.¹⁴ The severity of residual neuromuscular blockade varies with the type and number of variant alleles.

There are several diagnostic tests that can be used to diagnose PChE deficiency. One of the most commonly used is the dibucaine inhibition test. Dibucaine is a local anesthetic that inhibits ∼80% of PChE activity in normal individuals. Heterozygotes (individuals carrying 1 variant allele) will have PChE enzyme activity inhibited by approximately 40–60%. Homozygotes (individuals carrying 2 variant alleles) will have their enzyme activity inhibited by ∼20%. The percentage of inhibition is referred to as the dibucaine number; the lower the dibucaine number, the longer residual neuromuscular blockade can be expected to persist in patients administered SCh or mivacurium (Table 2). People who have acquired PChE deficiency, or people who are heterozygote carriers of a variant allele, typically will experience residual neuromuscular blockade for less than 2 hours. Homozygotes of a variant allele may experience residual neuromuscular blockade for up to 8 hours.^7,14 Serum plasma cholinesterase levels can be measured to show if a person has decreased PChE levels (normal levels range from 4000–13,500 U/L).¹⁷ This test, however, does not distinguish whether the deficiency is genetic or acquired.

Table 2.  .

Dibucaine Number and the Time of Neuromuscular Blockade

Pseudocholinesterase Allele	Dibucaine Number	Time of Blockade
Homozygous (usual or normal)	80	5–10 min
Heterozygous (variant)	40–60	up to 2 hurs
Homozygous (variant)	20–30	up to 8 h

Differential Diagnosis

When a patient fails to emerge from general anesthesia within a reasonable time, a differential diagnosis for the delayed emergence should be immediately formulated so that the cause of the problem can be identified and potentially corrected as soon as possible.¹⁵ If available, a cognitive aid should be used to assist or guide the anesthesia provider through the delayed emergence algorithm, ruling out each potential diagnosis until the most likely, or definitive diagnosis, remains (Table 3).³

Table 3.

Delayed Emergence Algorithm³

Check:

All inhalational and intravenous anesthetics have been turned off

There is no residual muscular paralysis

Monitors for signs of hypoxemia, hypercarbia, and hypothermia

For neurologic deficits (eg, anisocoria, asymmetric movement)

For hypoglycemia with a finger stick/glucometer

For medication swap or dosing error

If possible, obtain arterial blood gas plus electrolytes

Consider:

Opioid reversal: naloxone 40 μg or 0.5–1 μg/kg every 2 min (maximum 400 μg)

Benzodiazepine reversal: flumazenil 0.1–0.2 mg every 2 min (maximum 1 mg)

Scopolamine reversal: physostigmine 1 mg (beware of acute bradycardia)

Activation of emergency medical services

A reasonable algorithm for determining the underlying cause of delayed emergence should start with the confirmation that all anesthetic agents (both inhalational and intravenous) have been discontinued. It is also reasonable, early into the differential diagnosis algorithm, to check for residual neuromuscular blockade. Assuming the patient is still under general anesthesia, this can be easily performed with a peripheral nerve stimulator.³ If signs of wakefulness are evident (ie, eye opening, “bucking” on the endotracheal tube, purposeful responses to pain, a bispectral index value >60), the patient can be asked to follow simple commands such as blinking or squeezing the provider's hand.¹⁸ If a nondepolarizing agent has been used for neuromuscular blockade and evidence of residual neuromuscular blockade is present, then use of a reversal agent is indicated, such as an AChE inhibitor or cyclodextrin (ie, sugammadex). AChE inhibitors (eg, neostigmine, edrophonium, and physostigmine) function as reversible competitive antagonists of AChE, preventing the breakdown of ACh within the synaptic cleft of the neuromuscular junction.¹⁹ Sugammadex (Bridion), a novel drug introduced to the US market in 2015, works by encapsulating the intermediate-acting nondepolarizing neuromuscular blocking drugs rocuronium and vecuronium molecules, rendering them ineffective.²⁰

Diagnoses of delayed emergence can be further complicated by residual effects from previously administered opioids, benzodiazepines, or other anesthetic adjuncts capable of causing central anticholinergic syndrome (eg, scopolamine or atropine) or sedation (eg, diphenhydramine or promethazine). If indicated in an otherwise stable patient, opioid reversal can be considered by slowly titrating naloxone (40 μg or 0.5–1 μg/kg) every 2 minutes until miosis and respiratory depression are reduced or eliminated. Deliberate, cautious use of naloxone in this situation is necessary to avoid complications associated with opioid reversal including pain, tachycardia, hypertension, and pulmonary edema. Likewise, benzodiazepine reversal can be considered by carefully administering flumazenil (0.1–0.2 mg) every 2 minutes until signs of sedation are eliminated. If central anticholinergic syndrome is suspected, reversal with physostigmine (1 mg) is indicated with the understanding that severe bradycardia can ensue.³ Other agents with inherent sedative properties that lack any effective reversal options require time for the clinical effects to wane secondary to redistribution, metabolism, or elimination. While considering any pharmacologic causes of delayed emergence, all syringes and vials should be examined to rule out the possibility of a medication error (ie, accidental substitution or incorrect dosing).

Patients experiencing delayed emergence should also be evaluated for hypoglycemia, hypothermia, hypoxemia, and/or hypercarbia. If available, an arterial blood gas sample can be used to assess for any possible electrolyte abnormalities. The patient should be assessed for anisocoria, which may be a sign of a cerebral vascular accident. Evaluating the patient for any signs of focal neurological deficits is especially important in high-risk populations (eg, patients with hypertension, diabetes, age >75 years, history of transient ischemic attack/stroke). If deficits are noted, emergency medical services should be activated and the patient transported to a hospital for immediate computed tomography scan and full neurological evaluation.³

DISCUSSION

The main complication of PChE deficiency is prolonged neuromuscular paralysis leading to respiratory failure and subsequent hypoxia following administration of SCh or mivacurium.¹⁵ Therefore, patients who have received SCh or mivacurium as part of a general anesthetic should be thoroughly assessed for return of normal neuromuscular function prior to extubation. For patients who have known PChE deficiency or have a direct family member with the disorder, an alternative neuromuscular blocking drug other than SCh or mivacurium should be used.

Patients with or suspected of having acquired or genetic PChE deficiency should remain intubated with appropriate ventilatory support until spontaneous ventilation with adequate tidal volume is independently achieved. Patients should not be extubated until they have met all the requirements for safe extubation (Table 4).²¹ Furthermore, consideration should be given to ensure the patient remains appropriately sedated (ie, amnestic) until normal neuromuscular function is regained.

Table 4.

Criteria for Safe Extubation

Step 1: Plan extubation

Review the patient's preoperative airway findings

Consider the patient's comorbidities and associated risk factors

Consider surgical factors that may complicate the airway

Step 2: Prepare for extubation

Confirm that the patient is fully reversed from neuromuscular blockade

Train of four >0.9

Sustained hand grasp or head lift

Confirm that patient is adequately oxygenated

SpO2 >94%

Confirm that patient is breathing spontaneously

Respiration rate >8 bpm

Confirm that patient has adequate ventilation

Tidal volume >3–5 mL/kg

EtCO2 < 50 mm Hg

Confirm that the patient is hemodynamically stable

Confirm that the patient has emerged from stage 2 of anesthesia

Conjugate gaze

Pupils are normal

Confirm that the patient is neurologically intact

Patient follows verbal commands

Step 3: Perform extubation

Suction oral cavity and pharynx

Deflate endotracheal cuff

Apply positive pressure while removing endotracheal tube

Step 4: Recovery

Confirm airway patency

Apply 100% supplemental oxygen

Manage the airway as necessary

Monitor the patient's oxygenation and ventilation status

Confirm respiratory stability prior to discharge

The patient in this case most likely was a carrier of homogenous variant alleles of PChE. This is most readily indicated by the fact that she was not able to be extubated until 7.5 hours after SCh was administered during induction. Neither the patient nor her father had ever received general anesthesia; it was not known if her deceased mother had ever received general anesthesia. The patient was a descendant of Turkish parents who were born in a geographical location known to have a high incidence of PChE deficiency. Unfortunately, during postoperative discussions about the course of her anesthetic care and our high suspicion of her PChE deficiency, the patient patently refused the recommendation to schedule genetic testing for the disorder. She was discharged the day after surgery without undergoing any additional diagnostic or genetic tests.

CONCLUSION

PChE, or BChE, deficiency is a rare but serious complication of general anesthesia that can be caused by acquired or genetic factors. However, it is most commonly caused by a variant autosomal recessive gene and affects between 1 in 2000–5000 people, with a high incidence in certain populations. Persons with either form of PChE deficiency should not receive the neuromuscular blocking drugs SCh or mivacurium because these agents cannot be properly metabolized and are likely to result in prolonged residual neuromuscular blockade and subsequent delayed emergence from general anesthesia.

CONTINUING EDUCATION QUESTIONS

This continuing education (CE) program is designed for dentists who desire to advance their understanding of pain and anxiety control in clinical practice. After reading the designated article, the participant should be able to evaluate and utilize the information appropriately in providing patient care.

The American Dental Society of Anesthesiology (ADSA) is accredited by the American Dental Association and Academy of General Dentistry to sponsor CE for dentists and will award CE credit for each article completed. You must answer 3 of the 4 questions correctly to receive credit.

Submit your answers online at www.adsahome.org. Click on “On Demand CE.”

CE questions must be completed within 3 months and prior to the next issue.

• All of the following names have been used in the scientific literature to refer to the same enzyme except:

• 1. Acetylcholinesterase

  2. Butyrylcholinesterase

  3. Plasma cholinesterase

  4. Pseudocholinesterase.

• 2.The neuromuscular blockade action produced by succinylcholine is terminated once it is:

• 1. Broken down in the liver by CYP3A4 and CYP2D6 enzymes

  2. Disengaged from its receptor and moves into the neuromuscular junction

  3. Encapsulated by sugammadex and renally eliminated

  4. metabolized by acetylcholinesterase after leaving the N₁ACh receptor

• 3.Which of the following complications may occur when additional succinylcholine is administered immediately after an initial dose or if the initial dose exceeds 3–5 mg/kg?

• 1. Central anticholinergic syndrome

  2. Phase II block

  3. Prolonged fasciculations

  4. Tachycardia

• 4.Patients of the following descents all have a high incidence of pseudocholinesterase deficiency except:

• 1. Arya Vysya Indian

  2. Jewish-Persian

  3. Korean

  4. Turkish

• 5.The following are all considerations for managing a patient suspected of pseudocholinesterase deficiency who received succinylcholine during intubation except:

• 1. Administer sugammadex if residual neuromuscular blockade persists

  2. Ensure appropriate sedation and amnesia while the patient is paralyzed

  3. Keep the patient intubated and provide ventilatory support

  4. Refer for genetic or dibucaine inhibition testing