5: Peripheral nervous system

TOPIC 5 Peripheral nervous system



Topic Contents


Neuromuscular block monitor 87
Test: Train of four (TOF) stimulation 87

Investigation of suxamethonium apnoea 88
Test: Dibucaine and fluoride number 90

Test: Molecular genetic testing 91

Myasthenia gravis (MG) testing 92
Test: Edrophonium (tensilon) test 92

Test: Serum anti-acetylcholinesterase receptor antibody test 92

Test: Repetitive nerve stimulation (RNS) 92

Test: Single fibre electromyography (EMG) 93

Peripheral motor and nerve function assessment 94
Test: Nerve conduction studies and electromyography (EMG) 94


Neuromuscular block monitor



Test: Train of four (TOF) stimulation



Indications


Owig to the variable individual response and a narrow therapeutic window of muscle relaxants, a peripheral nerve stimulation test is recommended after their use. In particular:


• After long-acting neuromuscular block (NMB) drugs and prolonged infusions

• Pulmonary disease, obesity and neuromuscular disorders such as myasthenia gravis and Eaton-Lambert syndrome, myopathies

• When reversal agents are contraindicated, e.g. tachyarrythmias, liver and renal dysfunction.



How it is done



• Application of a supramaximal stimulus to a peripheral nerve, followed by measurement of the associated muscular response.

• The nerve stimulator device should generate a monophasic square wave constant current up to 80 mA, and last between 0.1 and 0.5 ms.

• The nerve chosen must be close to the skin, have a motor element and muscular contraction must be visible or accessible to monitoring.

• The negative electrode should be placed directly over the superficial part of the nerve and positive electrode placed proximally to avoid direct muscular stimulation.

• The generation of single, train of four, double burst and 50-Hz patterns of stimulation is necessary. Polarity of output should be marked, and battery powered for safety.

• Small surface electrodes are used to apply to overlying skin. Good electrical contact is essential.

• Monitoring in clinical practice is by visual and tactile responses.


Interpretation



• Different patterns of nerve stimulation are used to determine onset, offset and percentage of NMB.

• Relationship between receptor occupancy and evoked responses can be estimated.


Management principles



• Onset and offset of NMB is faster in central muscles with a good blood supply.

• The most accurate muscle to monitor during NMB onset and maintenance is the orbiclaris oculi as it will reflect the conditions of the central larynx and diaphragm muscles.

• It is best to monitor a peripheral muscle such as adductor pollicis during reversal as it has a longer recovery time than respiratory muscles and will provide a greater margin of safety.

• TOF ratio >0.9 correlates with the ability to protect the airway and swallow normally. However up to 75% of receptors still remain occupied at this point.

• Clinically significant residual paralysis is defined as TOF ratio <0.9.


Stimulus responses and abnormalities


See Table 5.1.



Table 5.1 TOF stimulation responses

image


Physiological principles




Limitations and complications



• Visual and tactile evaluation of muscular contractile response is unreliable. More accurate methods include mechanomyography (MMG), electromyography (EMG) and accelerometry (AMG) but they remain research tools.

• When monitoring is not performed up to 45% of patients are inadequately reversed on arrival to recovery room.

• When the T4–T1 ratio is 1 up to 50% of receptors can remain occupied (Table 5.2).

• Because of wide individual variability in responses, some patients may exhibit weakness at a TOF ratio of 0.8–0.9.

• Hypothermia increases skin impedance thus interpretation of evoked responses may be misleading.


Table 5.2 Receptor occupancy and TOF responses after neuromuscular paralysis

image


Investigation of suxamethonium apnoea


Suxamethonium is metabolized by the enzyme plasma cholinesterase (ChE). Abnormalities of this enzyme may cause prolonged muscular paralysis of variable duration after suxamethonium administration. The high prevalence of variant ChE genes in the population may contribute to the measured variability in recovery time after suxamethonium administration.


The clinical picture can be caused by (Table 5.3):


• Abnormal enzyme structure and activity

• Altered plasma enzyme concentration.

Table 5.3 Causes of suxamethonium apnoea





















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May 31, 2016 | Posted by in ANESTHESIA | Comments Off on 5: Peripheral nervous system

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Genetic variants Acquired causes
Atypical A Pregnancy
Fluoride resistant F Liver disease
Silent S Carcinomatosis
H (10% reduced concentration) Cardiac failure
J (33% reduced concentration) Uraemia