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• W4247644015 abstract "Mivacurium is a short-acting neuromuscular blocking drug that is rapidly degraded by serum cholinesterase [1]. Mivacurium may be the first choice for patients undergoing short procedures in day case surgery. In patients with a phenotypically abnormal serum cholinesterase, however, paralysis can be extremely prolonged [2-7]. Although very uncommon, unanticipated intense and prolonged neuromuscular blockade can be a problem in a busy ambulatory surgical center in which there are no facilities for long-term ventilation. In daily clinical practice, the patient's serum cholinesterase activity and phenotype are not normally known. Using a test dose has been suggested to identify individuals with a reduced ability to hydrolyze mivacurium. The administration of a test dose to predict unusual sensitivity toward mivacurium is controversial. In Baraka's article [6], a homozygote for the atypical gene was given a test dose of 15 [micro sign]g/kg mivacurium, and recovery to 10% of neuromuscular transmission was observed after 30 min. Ostergaard et al. [2], however, showed that 30 [micro sign]g/kg mivacurium can produce >2 h of complete paralysis in homozygotes for the atypical gene. To investigate the safety of a mivacurium test dose, we administered 14 [micro sign]g/kg mivacurium to a patient known to be homozygous for the atypical gene who was scheduled for an operation with an anticipated duration of approximately 1 h. Case Report A 19-yr-old patient was admitted for an elective bilateral thoracoscopic sympathicolysis because of excessive sweating of the hands and feet [8]. Her medical history included a prolonged response to succinylcholine administered during anesthesia for a tonsillectomy. She was a trained athlete, weighed 57.1 kg, and was 174 cm tall. She was taking a monophasic oral contraceptive containing 30 [micro sign]g of ethinyl estradiol plus 150 [micro sign]g of desogestrel [9]. The results of a general physical and a detailed neurological examination were unremarkable. The palms and the soles sweated profusely. Hyperhidrosis did not involve soft tissue swelling or deformities at the hands and the wrists. There were no congenital abnormalities [10,11]. The hematologic values, the urea nitrogen, creatinine, and glucose were normal. The serum sodium, potassium, ionized calcium, and magnesium concentrations were 135, 3.7, 1.05, and 0.9 mmol/L, respectively. Standard screening [12] to determine serum cholinesterase phenotype revealed that the patient was homozygous for the atypical variant (Table 1). DNA sequencing [13,14] was performed by the University of Nebraska Medical Center Molecular Biology Core Facility (Table 2). After obtaining written, informed consent and approval of the institutional ethics committee, a test dose of mivacurium was administered.Table 1: Serum Cholinesterase (ChE) PhenotypeTable 2: DNA Sequencing of the Gene Encoding for Serum Cholinesterase (ChE)After an overnight fast, the patient was premedicated with lorazepam 2.5 mg. Glycopyrrolate 0.2 mg and fentanyl 0.25 mg were given IV; 5 min later, anesthesia was induced with propofol 300 mg in divided doses. A left endobronchial tube was placed without the aid of a muscle relaxant. After intubation, 0.15 mg of fentanyl was administered. Anesthesia was maintained using a continuous infusion of propofol at a variable rate of 100-200 [micro sign]g [center dot] kg-1 [center dot] min (-1) titrated according to the hemodynamic response. The patient was ventilated with a fraction of inspired oxygen of 0.6 using intermittent positive pressure. The thoracoscopic procedure lasted approximately 45 min. At the end of the thoracoscopic sympathicolysis, the patient's palms and soles were dry. Postoperatively, the propofol infusion (100 [micro sign]g [center dot] kg-1 [center dot] min-1) and mechanical ventilation were continued until recovery of neuromuscular transmission. Neuromuscular transmission was evaluated by using evoked acceleromyography (TOF-Guard nerve stimulator; Biometer, Odense, Denmark) [15] on the right arm and by tactile evaluation of evoked twitch responses on the left arm. The patient's arms were adducted to 90[degree sign]. The stimulating current generated by the TOF-Guard consisted of supramaximal rectangular pulses (current intensity 60 mA, duration 200 [micro sign]s) into a train-of-four (TOF) pattern (frequency 2 Hz) and was delivered every 15 s to the ulnar nerve at the wrist via subcutaneous 27-gauge steel needle electrodes placed 30 mm apart. The hand and forearm were immobilized in supination and abduction on a splint, the thumb was allowed to move freely, and the fingers were strapped in extension. A piezoelectric ceramic transducer was attached on the top of the thumb with adhesive tape to measure acceleration during the contraction of the adductor pollicis muscle. As soon as the patient was intubated, baseline evaluation of neuromuscular transmission was started. The baseline reading of neuromuscular transmission was stable after 12 min; at this point, mivacurium 800 [micro sign]g (14 [micro sign]g/kg) was administered as an IV bolus, and the cannula was flushed with 10 mL of NaCl 0.9%. The time to complete ablation of twitch response was 197 s. During recovery from the neuromuscular block, the evoked responses to TOF stimulation were evaluated every 15-30 min at the left arm by touch. The stimulating current (60 mA) generated by a peripheral nerve stimulator (Innervator NS 242; Fisher & Paykel, Auckland, New Zealand) was applied to the ulnar nerve at the elbow by means of gelled silver-silver chloride skin electrodes. As the neuromuscular block dissipated, there was close correlation of the TOF count as measured by touch and by acceleromyography. At the end of the operation and approximately 4 h after mivacurium was administered, the patient was allowed to awake. This was done by discontinuing the propofol infusion for approximately 30 min. On both occasions, the patient was unable to move voluntarily. When the TOF ratio was recovered to 90% on the TOF-Guard, propofol administration was terminated. Approximately 7.5 h after the mivacurium administration, the patient was weaned successfully from the ventilator and made an uneventful recovery. Discussion Prolonged neuromuscular blockade caused by serum cholinesterase deficiency is a very uncommon anesthetic complication that requires specialized postoperative management and nursing care for successful treatment. It takes on added significance when it occurs in the ambulatory surgical patient. Busy ambulatory surgical centers may be particularly unsuited to coping with prolonged postoperative ventilation. Test doses have been proposed to identify those individuals with a reduced ability to hydrolyze muscle relaxants that are substrates for serum cholinesterase [6,16]. The administration of mivacurium 15 [micro sign]g/kg has been advocated as a screening test to predict unusual sensitivity to mivacurium in patients with unanticipated abnormal serum cholinesterase. Such a test dose is expected to produce a degree and duration of block that can be reversed easily with neostigmine [6]. However, information on the effect of very small doses in patients with inherited defects of serum cholinesterase is limited. To investigate the safety of a mivacurium test dose, we administered 14 [micro sign]g/kg mivacurium to a patient known to be homozygous for the atypical gene. In this patient, approximately one tenth of the normal mivacurium intubation dose induced complete paralysis for nearly 5 h (Table 3 and Figure 1).Table 3: Times to Recover from Mivacurium-Induced Neuromuscular BlockFigure 1: Tracing of the first twitch of the thumb after train-of-four stimulation of the ulnar nerve at the wrist after the administration of mivacurium 14 [micro sign]g/kg at time 0. The vertical axis shows the first twitch depression as percentage of prerelaxant control value. Assessment of neuromuscular transmission was performed using evoked acceleromyography.Neuromuscular block was quantified using accelerometry of the evoked thumb contraction. Although hyperhidrosis did not involve soft tissue swelling or deformities of the hands or forearms [10,11], a stainless steel needle, rather than skin surface electrodes, was used to apply the stimulating current to the ulnar nerve at the wrist. This was done to avoid problems with electrode contact and skin-to-electrode impedance due to the clammy skin. There were no problems in reaching supramaximal stimulation or in obtaining a prerelaxant baseline value. The first twitch response and TOF ratio recovered to the baseline value. The TOF count from the acceleromyogram at the right arm correlated with the number of palpable twitches after TOF stimulation at the left arm. Furthermore, clinical criteria of recovery were consistent with accelerometry responses. Therefore, it is unlikely that palmar hyperhidrosis prevented adequate assessment of neuromuscular transmission and that the prolonged block was an artifact based on deficiencies in the monitoring technique. The standard phenotyping procedures revealed a homozygous atypical variant of serum cholinesterase (Table 1). The DNA sequencing results are consistent with the interpretation that this patient has homozygous atypical serum cholinesterase (Table 2). The Asp 70 Gly mutation (abbreviated A for atypical) is characteristic of the atypical variant. This mutation is always present in people with the atypical phenotype [14]. The mutation, Ala 539 Thr (abbreviated K), is present as a second mutation in 90% of atypical alleles. Thus, most people with atypical phenotypes have two mutations in serum cholinesterase and are designated as having either an A/AK or AK/AK genotype [14]. Our patient has the A/AK genotype. Oral contraceptives, which are thought to reduce serum cholinesterase synthesis, have been reported to decrease serum cholinesterase activity by 50% [17,18] and may have further reduced enzyme activity in this patient. With usual serum cholinesterase type and average activity, most of the injected mivacurium molecules are destroyed before they can reach the endplate [19]. The lower the serum cholinesterase activity, the higher the proportion of drug molecules reaching the endplate and the more time it will take for the mivacurium concentration to become low enough for the endplate to resume function [20]. A review of the literature revealed that the reported times to reappearance of the first twitch response after the administration of mivacurium 30 [micro sign]g/kg ranged from 26 to 155 min in atypical patients [2,7]. Although the patient is homozygous for the atypical gene, it was surprising that such a small dose of mivacurium lasted so long. Like other relaxants, mivacurium undergoes a degree of renal excretion, and, even in the absence of enzymatic breakdown, distribution and renal elimination should have produced recovery from such a small dose earlier than was observed. Pharmacokinetic as well as pharmacodynamic factors could have contributed to the altered sensitivity to mivacurium in our patient. In addition to the failing enzymatic breakdown, enhanced susceptibility toward neuromuscular blocking drugs in general could have been present. Our patient was a trained athlete, and conditioning exercise shifts the dose-response curve for muscle relaxants to the left [21]. Furthermore, young women seem to be more sensitive to the effects of neuromuscular blocking drugs than age-matched men [22,23]. In this patient, mivacurium was very potent, much more so than mivacurium's structural relative, doxacurium. The more potent the drug, the longer the time to onset [24,25]. In this patient, the administration of 14 [micro sign]g/kg mivacurium was followed by complete suppression of twitch response within 197 s. The onset of neuromuscular blockade was relatively fast and comparable to that after 30 [micro sign]g/kg mivacurium in patients with homozygous atypical phenotypes from a previous investigation [2]. As a consequence of the failing enzymatic breakdown, the relative excess of mivacurium molecules to which the endplate was exposed could have accelerated the onset of neuromuscular block [25]. In conclusion, mivacurium test doses themselves may cause unanticipated prolonged apnea requiring postoperative ventilation for hours. Mivacurium should not be administered to patients with known serum cholinesterase deficiency, even in small doses. Neuromuscular monitoring and facilities for longterm ventilation should always be available in the recovery room whenever mivacurium is used." @default.
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• W4247644015 title "Prolonged Paralysis After a Test Dose of Mivacurium in a Patient with Atypical Serum Cholinesterase" @default.
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