[Reversal from non-depolarising neuromuscular blockade in the postoperative period]. / Ocena przewodnictwa nerwowo-miesniowego po operacjach wykonywanych w znieczuleniu ogólnym z zastosowaniem niedepolaryzujacych srodków zwiotczajacych.

BACKGROUND: Postoperative residual curarisation (PORC) is a serious and underestimated problem and may occur even after relaxation with medium-acting non-depolarising agents. METHODS: One hundred adult patients, scheduled for elective surgical procedures, were enrolled in the study. Atracurium or cis-atracurium was used for relaxation. Neostigmine was administered for reversal at the end of surgery, at the discretion of the attending anaesthesiologist. Neuromuscular transmission was not monitored in the operating room. In the recovery room, the presence of residual block was assessed by a blinded investigator using accelerometry (TOF-Guard, Organon, Holland) immediately after arrival (T-A) and after 45 min (T-B). Those who received neostigmine were allocated to group I (49 patients), and those who did not were allocated to group II (51 patients). RESULTS: The mean duration of anaesthesia was 92 min in group I and 103 min in group II. The respective doses of atracurium were 78.2 and 72.0 mg; and of cis-atracurium--17.6 mg and 18.0 mg. Immediately after arrival, a TOF below 0.7 was detected in 26% of patients, and below 0.9 in 48% of patients. After forty-five minutes the TOF was still below 0.7 in one patient and below 0.9 in seven. The number of patients with residual block (TOF<0.9) did not differ statistically between those who received neostigmine and those who did not (3.92% and 10.2%, respectively). CONCLUSION: The clinical assessment of neuromuscular blockade reversal did not allow for detection of PORC. Neostigmine was not fully effective in reversal.

Clinical evaluation of the Datex 221 neuromuscular transmission monitor for recording posttetanic electromyographic responses.

The assessment of deep neuromuscular blockade produced by nondepolarizing neuromuscular blocking agents is not possible with the conventional use of the Datex NMT-221 "relaxograph" (Datex NMT-221 monitor, Datex Instrumentarium, Helsinki, Finland), an otherwise useful electromyographic (EMG) monitoring device. A method whereby the relaxograph can be adapted to quantitatively measure posttetanic responses is described here. In anesthetized adult patients, neuromuscular blockade was monitored simultaneously on both hands with two relaxographs. On one hand, EMG responses of hypothenar muscles to the built-in 1/20-second sequence of train-of-four stimuli of the monitor were used. On the other hand, similar recordings were made with the addition of periodically superimposed supramaximal tetanic stimuli of 100 Hz to the ulnar nerve. Neuromuscular block was provided with pancuronium. The time courses of the spontaneous recovery of the first of the train-of-four EMG responses were compared in the stimulated and control arms. At the end of the surgery, the neuromuscular block was pharmacologically reversed with atropine and neostigmine. If no tetanic stimuli were applied, the EMG responses were identical in both arms during the spontaneous recovery from the neuromuscular blockade. If tetanic stimuli were applied every 4 or 7 minutes, the rate of recovery in the stimulated hand usually exceeded that of the control hand. However, no significant difference was observed in the recovery rate when the tetanic stimuli were spaced at 15-minute intervals. Pharmacologic reversal by atropine and neostigmine was found to be identical in all patient groups. The author concludes that the Datex relaxograph is suitable for the quantitative assessment of profound surgical neuromuscular blockade with the described modification.

Pancuronium requirements during hypothermic cardiopulmonary bypass in man.

Eight patients were studied to determine the changes in pancuronium requirements during hypothermic cardiopulmonary bypass. They were anaesthetised with fentanyl as the principal agent, ventilated with oxygen and the neuromuscular junction was monitored using train-of-four stimulation. After a bolus dose of pancuronium an infusion was used to maintain the first twitch of the train-of-four at 5-15 per cent of control. Before bypass the mean pancuronium infusion rate was 0.52 (SD 0.16) micrograms/kg/min. There was a small, brief increase in requirement with the initiation of bypass to 0.62 (SD 0.38) micrograms/kg/min, which was followed by a decrease of more than 80 per cent during hypothermia to 0.08 (SD 0.03) micrograms/kg/min. Rewarming was associated with a rapid increase in requirement to 0.64 (SD 0.17) micrograms/kg/min, which decreased to 0.33 (SD 0.23) micrograms/kg/min when normothermia was re-established.

Diuretic-induced hypokalaemia, pancuronium neuromuscular blockade and its antagonism by neostigmine.

The effect of hypokalaemia on a neuromuscular blockade induced by pancuronium and its antagonism by neostigmine was studied in the cat anterior tibialis-peroneal nerve preparation using the constant infusion of pancuronium technique. Hypokalaemia was induced by chronic administration of chlorothiazide. The infusion rate of pancuronium required to maintain a 90% depression of twitch tension was reduced from 0.72 +/- 0.06 microgram kg-1 min-1 in the cats with a normal serum concentration of potassium (K+ = 4.4 +/- 0.2 mmol litre-1; n = 7) to 0.41 +/- 0.07 microgram kg-1 min-1 in the hypokalaemic cats (K+ = 2.3 +/- 0.1 mmol litre-1; n = 8). The dose of neostigmine necessary for 50% antagonism of the pancuronium-induced depression of twitch tension (ED50) was 10.0 microgram kg-1 in the cats with a normal potassium concentration and 18.5 microgram kg-1 in hypokalaemic cats. We conclude that hypokalaemia decreases the dose of pancuronium required for neuromuscular blockade and increased the dose of neotigmine required for antagonism of the block.

Neuromuscular effects of respiratory and metabolic acid-base changes in vitro with and without nondepolarizing muscle relaxants.

The effects of metabolic (bicarbonate, [HCO3]) and respiratory (carbon dioxide, PCO2) acid-base changes on indirectly elicited twitch tension with and without nondepolarizing neuromuscular blocking agents were compared in a rat phrenic nerve-hemidiaphragm preparation. Ionized calcium [Ca2+] and magnesium [Mg2+] concentrations in the modified Krebs' solution were measured and kept constant. Likewise, twitch was altered when pH changes were produced by altering either PCO2 or [HCO3]. Decreasing pH either by increasing PCO2 or by decreasing [HCO3] significantly decreased (P less than 0.01) twitch, by 9.5 +/- 0.6 (SEM, n = 8) and 10.6 +/- 1.5%, respectively. Increasing pH by decreasing PCO2 or by increasing [HCO3] significantly increased (P less than 0.01) twitch, by 5.6 +/- 0.9 and 7.9 +/- 0.6%, respectively. After a partial depression of twitch by nondepolarizing neuromuscular blocking agents, the effects of PCO2 and [HCO3] changes were again assessed. Decreasing pH by increasing PCO2 or by decreasing [HCO3] intensified d-tubocurarine (dTc) (28.2 +/- 1.6 and 32.0 +/- 2.9%, respectively) and vecuronium (23.0 +/- 1.4 and 36.8 +/- 3.2%, respectively) block, whereas it reversed metocurine (1.2 +/- 2.2% NS and 2.9 +/- 1.3%, respectively) and pancuronium (8.3 +/- 1.5 and 11.5 +/- 3.0%, respectively) block. Conversely, increasing pH by decreasing PCO2 or by increasing [HCO3] antagonised dTc (12.8 +/- 2.2 and 13.6 +/- 1.8%, respectively) and vecuronium (25.3 +/- 1.7 and 25.0 +/- 3.0%, respectively) block, whereas it potentiated metocurine (4.2 +/- 0.6 and 8.0 +/- 1.1%, respectively) and pancuronium (11.0 +/- 1.2 and 17.5 +/- 2.0%, respectively) block. Except where indicated, all changes in block described above were statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Monitoring of curarisation in patients with tetraparesis.

Neuromuscular blockade induced by pancuronium was monitored on the trapezius and abductor digiti minimi muscles in three patients with upper motor neurone lesions: one patient was hemiparetic and two were tetraparetic. A greater sensitivity to pancuronium was always observed on the trapezius muscle. It is suggested that the assessment of curarisation is more reliable on proximal than on distal muscles if the patient's sensitivity to relaxants is expected to be generally low.

Neurophysiological monitoring of pharmacological manipulation in acute organophosphate (OP) poisoning. The effects of pralidoxime, magnesium sulphate and pancuronium.

OBJECTIVES: The neuromuscular transmission failure in acute organophosphate (OP) poisoning occurs because of the irreversible inactivation of the enzyme acetylcholinesterase located in the neuromuscular junction, and is distinguished neuroelectrophysiologically by single electrical stimulus-induced repetitive responses and either a decremental or a decrement-increment response upon high-rate repetitive nerve stimulation (RNS). Understandably, the administration of pharmacological agents with actions at different sites in the neuromuscular junction would alter the neuroelectrophysiological findings in acute OP poisoning. METHODS: The effect of several pharmacological agents including pralidoxime (10 patients), magnesium sulphate (4 patients) and pancuronium (7 patients) on the neuroelectrophysiological abnormalities was studied in 21 patients with acute OP poisoning. RESULTS: Pralidoxime administration produced neurophysiological amelioration in 11 out of 15 occasions. In those cases where it produced a beneficial effect, pralidoxime administration was continued and its neuroelectrophysiological effects were studied daily. The efficacy of pralidoxime administration was demonstrated by neuroelectrophysiological testing for a maximum of 6 days after poisoning. Three types of neuroelectrophysiological responses to pralidoxime were noted: (i) lack of neuroelectrophysiological improvement (two patients); (ii) initial improvement with subsequent lack of improvement (two patients); and (iii) initial improvement with subsequent normalisation of neuromuscular transmission (5 patients). Normalisation of the electrodiagnostic tests and the failure of pralidoxime to ameliorate the neuromuscular transmission abnormalities were neuroelectrophysiological indications for the discontinuation of pralidoxime treatment. The administration of magnesium sulphate (MgSO4.7H2O, 4 g intravenous) resulted in a decrease in the CMAP amplitude, loss of the repetitive response and conversion of the decrement-increment response at high-rate RNS to an incremental response. Repetitive responses and the decremental response at high-rate RNS also disappeared after the administration of pancuronium (0.5 mg intravenous) to 6 patients. However, in one case where pancuronium administration was preceded by pralidoxime, there occurred a dramatic worsening of the neuromuscular transmission defect. CONCLUSIONS: While the administration of all 3 agents-- pralidoxime, magnesium sulphate and pancuronium-- resulted in the reversion of the neuroelectrophysiological defects, only pralidoxime is contended to be therapeutically useful. The therapeutic benefit due to its administration is limited by a short duration of action, and hence it is recommended that it should be administered for a longer period of time under neuroelectrophysiolgical guidance.

Acute necrotizing myopathy of intensive care: electrophysiological studies.

A series of recent reports have identified cases of a quadriplegic myopathy characterized by myofiber necrosis and loss of myosin filaments associated with the use of nondepolarizing muscle blocking agents and glucocorticoids. We report electrophysiological findings in 7 intensive care unit patients who developed evidence of an acute myopathy in association with the use of nondepolarizing muscle blocking agents. Several important features were identified: (i) a neuromuscular transmission deficit was observed in 3 patients up to 7 days following withdrawal of vecuronium; (ii) motor M potentials were of low amplitude, there was mild abnormal spontaneous activity on needle electromyography, and sensory conduction was relatively preserved; (iii) not all patients received glucocorticoids or were asthmatic; (iv) 2 patients given vecuronium had very high creatine kinase levels and developed acute renal failure associated with myoglobinuria; and (v) rises in motor M potentials accompanied clinical recovery. This complication of intensive care may be severe, but is reversible and possibly avoidable. Our findings implicate nondepolarizing muscle blocking agents in the development of the myopathy. Electrophysiological studies provide important prognostic guidance.

[Influence of pavulon on facial nerve monitoring during middle ear-mastoid operation].

OBJECTIVE: To evaluate the influence of pavulon (muscle relaxant) on facial nerve monitoring for patient with middle ear-mastoid operation during general anesthesia. METHOD: Intraoperative monitoring of the facial nerve (FNM) was done in 45 ears (44 case). For patient with middle ear-mastoid disease, 38 ears underwent inhaled-intravenous anesthesia with muscle relaxant pavulon (group of general anesthesia), 7 ears underwent local anesthesia (group of local anesthesia). Accelography (ACCG) was used in 10 case for testing the correlation between of FNM and the various degree of recovery from ulnar nerve-musculor blockade. RESULT: FNM could be elicited during different periods of recovery with values of T4/T1 varying from 10%-98%. Pavulon could be used to eliminate muscular vibration from disturbing FNM. Electromyography (EMG) potentials were successfully recorded in 34 ears (89.4%). Anesthesia was uneventful and it may be controled satisfactority. CONCLUSION: Considering the advantage of pavulon. It can be used for general anesthesia during intraoperative monitoring of the facial nerve for children or adults suffering from local complicated diseases.