Neuromuscular monitoring in intensive care patients: milliamperage requirements for supramaximal stimulation{dagger}

N. J. N. Harper, R. Greer and D. Conway

Manchester Royal Infirmary, Oxford Road, Manchester M13 9WL, UK*Corresponding author

{dagger} 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


    Abstract
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 Abstract
 Introduction
 Materials and methods
 Comment
 References
 
We investigated the effects of peripheral oedema on the supramaximal current required for neuromuscular monitoring of critically ill patients. We studied 32 sedated patients who had not needed a neuromuscular blocking drug. The presence of oedema over the volar aspect of both wrists was assessed by a blinded observer and graded (grade 0, no oedema; grade 1, mild oedema; grade 2, gross oedema). The supramaximal current was derived by applying an incrementally increasing current over the ulnar nerve and measuring the amplitude of the electromyographic (EMG) response of the first dorsal interosseous muscle. The supramaximal current was that current above which there was no significant increase in EMG amplitude. It was 40 mA in the absence of oedema. This current was significantly increased in the presence of grade 1 oedema (60 mA, Mann–Whitney test, P<0.01) and grade 2 oedema (82.5 mA, Mann–Whitney test, P<0.01). In the presence of oedema, the required supramaximal current decreased significantly after the application of pressure over the stimulating electrodes (Wilcoxon signed rank test, P<0.05). Supramaximal current in critically ill patients is increased in the presence of peripheral oedema. We recommend that nerve stimulators used for neuromuscular monitoring in the ICU are capable of delivering a stimulus current of at least 100 mA.

Br J Anaesth 2001; 87: 625–7

Keywords: intensive care; monitoring, neuromuscular function, supramaximal stimulus; equipment, neuromuscular monitor


    Introduction
 Top
 Abstract
 Introduction
 Materials and methods
 Comment
 References
 
The effects of neuromuscular blocking agents may be more variable in critically ill patients because of changes in their pharmacokinetics and pharmacodynamics. It is important to monitor the effects of these drugs so that paralysis is adequate but excessive doses of drug are avoided.

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 50–60 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


    Materials and methods
 Top
 Abstract
 Introduction
 Materials and methods
 Comment
 References
 
After obtaining Ethics Committee approval, we studied 32 intensive care patients who were mechanically ventilated. Sedation was standardized using a well-established scoring system based on the Ramsay score. No patient received a neuromuscular blocking agent before or during the period of assessment. Plasma electrolyte concentrations and core-periphery temperature gradient were recorded. A blinded observer (N.J.N.H.) graded the presence of oedema on both wrists. Grade 0 indicated no oedema, grade 1 mild oedema, and grade 2 gross oedema. Hand dominance was noted.

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. Spearman’s 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, Mann–Whitney test) and in the presence of grade 2 oedema it was 82.5 mA (median, P<0.01, Mann–Whitney 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 0–100 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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Fig 1 Milliamperage current (mA) required for supramaximal stimulation in critically ill patients with differing grades of peripheral oedema. Median currents supramaximal current are depicted as a horizontal line before the application of pressure (light shading) and after the application of pressure (dark shading). The limits of the box represent the 25th and 75th percentiles and the bars represent the range. Individual patients with current requirements greater than 100 mA are indicated as O. The median supramaximal current was 40 mA in non-oedematous limbs. In comparison with the non-oedematous state, the supramaximal current in the presence of oedema was significantly raised (P<0.01, Mann–Whitney test): grade 1 oedema median supramaximal current=60 mA and grade 2 oedema median supramaximal current=82.5 mA. The application of pressure (dark shading) made no difference to the supramaximal current C where there was no oedema, but it decreased significantly (Wilcoxon signed rank test, P<0.05) to 50 mA in the presence of grade 1 oedema and to 75 mA in the presence of grade 2 oedema (Wilcoxon signed rank test, P<0.05).

 

    Comment
 Top
 Abstract
 Introduction
 Materials and methods
 Comment
 References
 
The use of neuromuscular blocking drugs in intensive care is common and the incorrect monitoring of neuromuscular function may lead to inappropriate clinical decisions. The ability to monitor neuromuscular function correctly depends upon delivering a supramaximal current at which all muscle fibres respond to the applied stimulus. Failure to deliver this current may make assessment difficult or may lead to an overestimation of the degree of neuromuscular block. In addition, critically ill patients may exhibit altered sensitivity to these agents.4

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 50–60 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.


    Acknowledgements
 
We would like to acknowledge Sally Hollis, Senior Lecturer in the Department of Medical Statistics, University of Lancaster for her help in the analysis of the data.


    References
 Top
 Abstract
 Introduction
 Materials and methods
 Comment
 References
 
1 Kopman AF, Lawson D. Milliamperage requirements for supramaximal stimulation of the ulnar nerve with surface electrodes. Anesthesiology 1984; 61: 83–5[ISI][Medline]

2 Plank LD, Hill GL. Modern techniques for measuring body composition in patients who are critically ill. In: Bion J, ed. Current Topics in Intensive Care. London: W.B. Saunders 1995; 125–144

3 Sliwa JA. Acute weakness syndromes in the critically ill patient. Arch Phys Med Rehab 2000; 81: S45–S52[ISI][Medline]

4 Harper NJN. Neuromuscular blocking drugs: practical aspects of research in the intensive care unit. Intensive Care Med 1993; 19: S80–S5[ISI][Medline]

5 Brull SJ, Silvermann DG. Pulse width, stimulus intensity, electrode placement, and polarity during assessment of neuromuscular function. Anesthesiology 1995; 83: 702–9[ISI][Medline]

6 Beemer GH, Reeves JH. An evaluation of eight peripheral nerve stimulators for monitoring neuromuscular blockade. Anaesth Intensive Care 1988; 16: 464–77[ISI][Medline]





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