Manchester Royal Infirmary, Oxford Road, Manchester M13 9WL, UK*Corresponding author
This work was presented in part at the Anaesthetic Research Society meeting in November 2000 at the Hammersmith Hospital, London.
Accepted for publication: June 4, 2001
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Abstract |
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Br J Anaesth 2001; 87: 6257
Keywords: intensive care; monitoring, neuromuscular function, supramaximal stimulus; equipment, neuromuscular monitor
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Introduction |
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Neuromuscular monitoring relies on the application of a supramaximal current so that the response of all motor units is assessed. The supramaximal current is the current above which there is no increase in the evoked muscle response. At this stimulus current, all motor units are firing in response to nerve stimulation. A current of 5060 mA provides supramaximal stimulation in all patients during anaesthesia.1 Should a supramaximal stimulus not be achieved then the degree of neuromuscular block may be overestimated and subsequent clinical decisions may be inappropriate.
Critically ill patients commonly develop peripheral oedema largely as a result of the development of an increased extracellular fluid volume.2 Patients may also develop a marked core-periphery temperature gradient as a result of hypoperfusion. These physiological changes might be expected to alter the current required for supramaximal stimulation by increasing the electrical impedance of the tissues. Furthermore, the development of critical illness polyneuropathy may reduce the amplitude of the induced action potentials.3
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Materials and methods |
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Electromyographic (EMG) studies were performed by stimulating the ulnar nerve and recording the EMG amplitude over the first dorsal interosseous muscle. In all cases, the recordings were made using the Dantec Neurostim 2000® electromyograph. The site of stimulation was prepared with acetone and ECG-type electrodes were placed over the ulnar nerve at the wrist. The recording electrode was placed over the first dorsal interosseous muscle. The hand was then thermally insulated. Thumb skin temperature was recorded.
The polarity of the stimulating current applied over the ulnar nerve was consistent; we used a signal with a square waveform and duration of 0.2 ms. In all cases the cathode was distal. The stimulating current was applied in a graded fashion, increasing from 0 to 100 mA in 5 mA increments over approximately a 10 min period. The amplitude of the EMG response was recorded and measured on the display using cursors. The process was then repeated after the application of continuous pressure over the stimulating electrodes. In each patient, measurements were made in both the dominant and the non-dominant hands. The pressure was applied for 15 s before the start of repeat measurements and for the duration of these measurements. The supramaximal stimulus was that current above which there was no significant increase in recorded EMG amplitude despite an increase in current applied.
As our data was categorical and the supramaximal current was greater than the maximum current deliverable by our apparatus in a small number of patients, we applied non-parametric tests to our data, which were analysed using SPSS (Windows 95 version 7). We applied the Mann Whitney test to compare the supramaximal current between groups. The Wilcoxon signed rank test was used to assess any effect of pressure or hand dominance on the supramaximal current. Spearmans rank correlation and analysis of covariance were applied to assess the effect of core-periphery temperature gradient in the presence of oedema.
In eight patients the grade of oedema was different in each hand, irrespective of hand dominance. The data from each patient were, therefore, not aggregated and the recordings from each hand were analysed separately so that 32 patients yielded 64 sets of data.
The median supramaximal current was 40 mA in non-oedematous limbs. In comparison with the non-oedematous state, the presence of grade 1 oedema was associated with a significantly raised supramaximal current (median 60 mA, P<0.01, MannWhitney test) and in the presence of grade 2 oedema it was 82.5 mA (median, P<0.01, MannWhitney test). The application of pressure made no difference to the supramaximal current where there was no oedema, but the supramaximal current decreased significantly to 50 mA in the presence of grade 1 oedema (Wilcoxon signed rank test, P<0.05) and to 75 mA in the presence of grade 2 oedema (Wilcoxon signed rank test, P<0.05) (Fig. 1). When pressure was not applied, there were five supramaximal current values greater than 100 mA but after the application of pressure all values fell within the 0100 mA range. Hand dominance did not affect the supramaximal current (Wilcoxon signed rank test). There was no relationship between supramaximal current and the core-periphery temperature gradient (r=0.2, P=0.26). There was no evidence of an effect of oedema on this relationship (analysis of covariance P=0.9).
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Comment |
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In order to elicit the stimulation of a nerve it is important to deliver an adequate electrical charge. Charge is the product of current intensity (mA) and pulse width (ms). The current intensity generated by a nerve stimulator is directly related to the emitted voltage and inversely related to the impedance (I=V/R). It has been demonstrated clinically that in assessing neuromuscular function the ability to deliver this current consistently is related to the pulse width, electrode placement and polarity.5 In our study, all these factors were consistent. The Dantec Neurostim 2000® electromyograph has the ability to deliver a constant current over a wide range of impedance.
Kopman and Lawson1 demonstrated that a stimulus of 5060 mA is required for supramaximal stimulation in a population of anaesthetized patients. In a population of critically ill patients without peripheral oedema we found the same stimulus current was required. However, the presence of oedema increases the current required for supramaximal stimulation. For patients with grade one oedema 60 mA was required and for patients with grade 2 oedema, 82.5 mA was required. A possible explanation is that the presence of oedema decreases the current density available for stimulation of the nerve. The application of pressure significantly reduced the supramaximal current for patients with oedema by approximating the stimulus to the nerve and increasing the available charge. Without the application of pressure, there were a number of patients for whom the supramaximal current was greater than the maximum output of the electromyograph (100 mA). After the application of firm pressure over the stimulating electrodes, the SMC was within the 100 mA range.
Beemer and Reeves evaluated eight neuromuscular monitors and demonstrated that only three (Fisher Paykel A400, Myotest DBS, and Rutter 4B) were able to deliver a constant current over a wide range of skin impedance and that of those the highest deliverable current was 86 mA.6 We have demonstrated that in critically ill patients a supramaximal stimulus may require a higher current and that peripheral oedema may impair accuracy of neuromuscular monitors in this environment. The mechanism for the increase in supramaximal current is likely to be a dissipation of current in oedematous tissues. The actual current presented at the nerve is unknown and we advise caution in the application of large currents for neuromuscular monitoring.
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Acknowledgements |
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References |
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