A Case of Pseudocholinesterase Deficiency in the PACU

Leadingham, Camille

doi:10.1016/j.jopan.2007.05.005

Cited by 12 publications

(20 citation statements)

References 11 publications

(33 reference statements)

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“…However, if prolonged paralysis does occur, the patient is usually admitted to the ICU for extended intubation and mechanical ventilation. [1][2][3][4][5][6] Succinylcholine and mivacurium are NMBAs of choice when only a very short period of paralysis is needed. Recovery from succinylcholine paralysis starts within 2 to 3 minutes, and recovery from mivacurium paralysis begins within approximately 5 to 10 minutes.…”

Section: Discussionmentioning

confidence: 99%

“…Abnormalities in potassium, magnesium, or calcium levels can contribute to the impaired function of plasma cholinesterase. 2 At this time, the reversal of paralysis due to succinylcholine or mivacurium by using drugs that inhibit plasma cholinesterase and are also used for nondepolarizing NMBAs that are not dependent on plasma cholinesterase for metabolism is not recommended because of the potential for intensified neuromuscular blockade. Furthermore, residual blockade may be only several hours long, and exposure of patients to muscarinic side effects of increased acetylcholine levels such as bradycardia, excessive oral and pulmonary secretions, and vomiting may not be warranted.…”

Section: Monitoring Effects Of Nmbasmentioning

confidence: 99%

“…1,5,16 Use of fresh frozen plasma to reverse paralysis is questionable because the reversal from the small amount of plasma cholinesterase contained in fresh frozen plasma is usually transient and multiple units may be required to keep the paralysis adequately reversed. 2 Whether or not reversal of paralysis is attempted, the primary plan of www.ajcconline.org • Drug blocks the acetylcholine receptor and prevents binding to the postsynaptic acetylcholine receptor. Drug prevents depolarization of plasma membrane of motor end plate and muscle contraction.…”

Section: Monitoring Effects Of Nmbasmentioning

confidence: 99%

“…[1][2][3][4][5][6][7][8][9]18 Nurses should recognize and report an abnormal dibucaine inhibition number and plasma cholinesterase levels. Additionally, nurses should not hesitate to discuss referral for genetic consultation when the dibucaine inhibition number is less than 80%.…”

Section: Nursing Skill Rationalementioning

confidence: 99%

“…Patients with plasma cholinesterase deficiency are at risk for toxic effects from other drugs that undergo plasma cholinesterase metabolism such as tetracaine, procaine, and cocaine. 2 No evidence is currently available to support the routine practice of genetic screening for deficiency in plasma cholinesterase in order to predict an individual's response to NMBAs such as succinylcholine or mivacurium. To better understand the pharmacogenomics of this enzyme deficiency, consulting with a medical geneticist with experience in pharmacogenomics would be especially useful.…”

Section: Nursing Skill Rationalementioning

confidence: 99%

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Prolonged Paralysis and Apnea After Receiving a Neuromuscular Blocking Agent: What Nurses Should Know

Jaramillo

Scruth

Cheng

2009

American Journal of Critical Care

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After receiving mivacurium, a short-acting neuromuscular blocking agent used for intubation before surgery, a patient experienced prolonged paralysis and prolonged apnea that required ventilator support. Although this complication is rare, all critical care nurses should be aware of it so they can be competent in managing and providing holistic and comprehensive nursing care to the patient and the patient's family. Although this complication has been documented in the anesthesia literature, it has received little mention in critical care nursing journals. (American Journal of Critical Care. 2009;18:592,588-591) T his case report describes a patient who had prolonged paralysis and apnea after receiving mivacurium, a neuromuscular blocking agent (NMBA), for endotracheal intubation before surgery. This rare perioperative complication occurs in patients with plasma cholinesterase (pseudocholinesterase) deficiency. Most reported cases of prolonged paralysis are in patients receiving succinylcholine. In this case report, we discuss the use of both depolarizing and nondepolarizing muscle relaxants that undergo metabolism by plasma cholinesterase and the following critical care nursing issues: providing competent care for patients receiving NMBAs, management of acute prolonged paralysis and apnea, management of suspected plasma cholinesterase deficiency, strategies for prevention and patient safety, and future objectives for research. Case ReportA 56-year-old woman with a below-the-knee amputation of the right lower extremity was readmitted to the hospital for treatment of a 1-week-old stump that was dehisced and infected due to injury. Her medical history included chronic kidney disease treated with peritoneal dialysis, congestive heart failure, hypertension, neuropathy, peripheral vascular disease, diabetes, and malnourishment. The plan Continued on page 588Cases of Note features peer-reviewed case reports and case series that document clinically relevant findings from critical and high acuity care environments. Cases that illuminate a clinical diagnosis or a management issue in the treatment of critically and acutely ill patients and include discussion of the patient's experience with the illness or intervention are encouraged. Proposals for future Cases of Note articles may be e-mailed to ajcc@aacn.org. After induction and the start of maintenance anesthesia, the train of four (TOF) delivered by the peripheral nerve stimulator was 0 out of 4 twitches, indicating complete paralysis or 100% blockage of the acetylcholine receptors at the motor end plate. Because the patient's TOF did not return as expected and neuromuscular blockade could not be reversed, the surgical procedure was deferred and the patient was transferred to the intensive care unit (ICU) still intubated and mechanically ventilated for recovery from anesthesia. The prolonged paralysis was assumed to be due to plasma cholinesterase deficiency that resulted in extremely slow metabolism of mivacurium. By day 3, the patient's paralysis had compl...

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