Anaesthesia, 1992, Volume 47, pages 2 17-21 9

Suxamethonium block in the myasthenic patient

Correlation with plasma cholinesterase

A. BARAKA

Summary
The neuromuscular block of suxamethonium 1.5 mg.kg- was investigated in three myasthenic patients (Class I I A ) , undergoing
thymectomy. Two of the patients were receiving pre-operative pyridostigmine therapy. In the three patients, plasma
cholinesterase activity was determined on the morning of surgery and was correlated with the neuromuscular response to
suxamethonium as monitored by electromyography. The results suggest that the response to suxamethonium in the myasthenic
patients can show wide variations according to the level of their plasma cholinesterase activity. The degree and duration of
suxamethonium block is inversely related to the plasma cholinesterase activity.

Key words
Neuromuscular relaxants; suxamethonium.
Complications; myasthenia gravis.

Resistance to suxamethonium has been shown in the myas- plasma cholinesterase activity was measured in the three
thenic patient [l], and in those with ocular myasthenia the patients, using spectrophotometry and pro-prionylthiocho-
resistance seems to be in the uninvolved muscles [2]. line as a substrate [8]. Also, dibucaine numbers were
However, myasthenic patients during a true remission may determined.
not demonstrate resistance [3]. Treatment of myasthenic Neuromuscular transmission was monitored in the oper-
patients by anticholinesterases can decrease plasma cho- ating theatre by electromyography by a Datex Relaxograph
linesterase activity and delay the hydrolysis of suxa- (R) monitor. The ulnar nerve was stimulated supramaxi-
methonium [4, 51. Thus, myasthenic patients treated with mally at the wrist every 20 s, and the resulting electromyo-
anticholinesterases may exhibit a prolonged suxametho- graphic response displayed. The monitor uses the train-of-
nium neuromuscular block, although this is poorly four principle a t a stimulus frequency of 2 Hz, and
documented [6]. computes the ratio of the fourth to the first evoked
The present report investigates the neuromuscular block response (T4/T1 ratio), as well as the Tl/control ratio.
of suxamethonium in three myasthenic patients, and corre- The three patients were premedicated with intramuscular
lates the response with plasma cholinesterase activity. atropine 0.6 mg and oral diazepam 5 mg. Anaesthesia was
induced with thiopentone 5 mg.kg-l. Following induction
of anaesthesia and while the patients were breathing 100%
Method
oxygen, the electromyographic response was recorded.
Investigation was carried out in three myasthenic patients When a steady response was achieved, suxamethonium
undergoing thymectomy via midsternotomy. The three 1.5 mg.kg- was injected intravenously and the neuro-
patients were suffering from generalised myasthenia gravis muscular response was monitored. When maximal neuro-
(Osserman grade 1 IA) [7]. Patients data are presented in muscular block was achieved, the trachea was intubated,
Table 1. and anaesthesia was maintained with 65% nitrous oxide in
Patients were medically treated prior to thymectomy for oxygen supplemented by 5 pg.kg- fentanyl. The degree of
2-6 months. In the first patient, no anticholinesterase block achieved by suxamethonium and the time required
therapy was used, while oral pyridostigmine 60 mg for 75% recovery of Tl/control ratio was recorded.
6 hourly, was used in the second and third patients. Following recovery from suxamethonium blockade,
Pyridostigmine was discontinued the evening of surgery in incremental doses of 0.01 mg.kg- vecuronium were used
the second patient, and was continued until the morning of to maintain muscle relaxation throughout surgery. At the
surgery in the third patient. On the morning of surgery, termination of surgery, residual neuromuscular blockade

A. Baraka, MB, BCh, DA, DM, MD, FCAnaes (Hon.) Professor and Chairman, Department of Anesthesiology, American
University of Beirut, Beirut, Lebanon.
Accepted 5 August 1991.

0003-2409/92/0302 17 + 03 $03.00/0 @ 1992 The Association of Anaesthetists of G t Britain and Ireland 217
218 A . Baraka

Table 1. Patient data. Table 3. This shows the plasma cholinesterase activity and the
~~ corresponding time to 75% recovery of the Tl/control ratio.
Patient Age (years) Sex Classification Treatment
Plasma cholinesterase
I 14 F IIA Plasmapheresis (3 sessions) Patient activity (U.mlF') Recovery time (min)
Prednisone 25 mg.day-'
Azathioprine 150 mg.day-' I 5. I6 3
2 30 F IIA Pyridostigmine 60mg 2 I .45 16
6 hourly 3 0.73 35
3 67 M IIA Pyridostigmine 60mmg
6 hourly

Suxamethonium neuromuscular block

Table 2. The plasma cholinesterase activity and the dibucaine
number in the three patients. Normal value in our population is As shown in Figure 1, suxamethonium 1.5 mg.kg-' did not
2.5-6 unitsm- I. result in complete neuromuscular block in the first patient.
Also, 75% recovery of the Tl/control ratio was rapidly
Plasma cholinesterase achieved after 3 min. In the other two patients, suxametho-
Patient activity (U.rn1-I) Dibucaine number nium produced complete neuromuscular blockade.
Seventy-five percent recovery of Tl/control ratio was
I 5.16 90 achieved after 16min in the second patient and after 35
2 I .45 90
3 0.73 88 min in the third patient.
The recovery times in the three patients were inversely
related to their plasma cholinesterase activity (Table 3).
was reversed by a mixture of neostigmine 0.05 mg.kg-' and
atropine 0.02 mg.kg-'. Discussion
Myasthenia gravis is an autoimmune disease that results
Results from the production of autoantibodies against the acetyl-
choline receptors of the neuromuscular synapse, with sub-
Plasma cholinesterase
sequent reduction in the functional endplate receptors.
As shown in Table 2, the plasma cholinesterase was normal Reduction in the number of receptors is brought about
in the first patient who was not receiving pyridostigmine. In either by an increased rate of degradation, or by functional
the second patient whose anticholinesterase therapy was blockade [9].
discontinued the evening of the surgery, the plasma cho- The decreased number of endplate receptors can decrease
linesterase was moderately decreased, while it was the response to the chemical transmitter acetylcholine, as
markedly decreased in the third patient whose therapy was well as to the depolarising action of decamethonium [lo]
continued till the morning of surgery. In the three patients, and suxamethonium [ 1,2]. This can explain the resistance
the dibucaine number was within the normal range to suxamethonium block which was observed in the first
denoting homozygous typical enzyme [E,"E, "1. myasthenic patient who was not treated by anticholinester-

Suromethonium
1.5 rnq.kg-'
Fig. 1. Electromyographic response to ulnar nerve stimulation by a train-of-four every 20s, showing the effect of suxamethoniurn
1.5 mg.kg-'. In the first patient (upper tracing), only partial block was achieved and 75% recovery of Tl/control ratio was observed after
3 min. In the second patient (middle tracing), complete block was achieved and 75% recovery was observed after 16 min. In the third patient
(lower tracing), 75% recovery was achieved after 35 min.
 Suxamethonium block in the myasthenic patient 219

ases. In the other two patients treated with pyridostigmine, [2] BARAKA A, AFIFIA, MUALLEM M, KACHACHI T, FRAYHAF.
suxamethonium produced complete and prolonged neuro- Neuromuscular effects of halothane, suxamethonium and
tubo-curarine in a myasthenic undergoing thymectomy.
muscular block. British Journal of Anaesthesia 1971; 4 3 91-5.
The different response to suxamethonium in the three [3] ABEL M, EISENKRAFTJB, PATEL N . Response to
myasthenic patients may be attributed to the different suxamethonium in a myasthenic patient during remission.
plasma cholinesterase activity. The plasma cholinesterase Anaesthesia 199 I ; 46: 30-2.
[4] BARAKAA, WAKIDN, MANSOURR. HAVDAVW. Effect of
activity was normal in the first patient, while it was moder-
neostigmine and pyridostigmine o n the plasma cholinesterase
ately decreased in the second patient and markedly reduced activity. British Journal of Anaesthesia 1981; 5 3 849-51.
in the third patient. Anticholinesterases have been shown [5] BARAKA A. Suxamethonium-neostigmine interaction in
to decrease the plasma cholinesterase activity [4], and hence patients with normal or atypical cholinesterase. British
can result in decreased hydrolysis of suxamethonium with a Journal of Anaesthesia 1977: 4 9 479-84.
[6] DIERDORFSF. Rare co-existing diseases. In: BARASHPG,
subsequent potentiation of its neuromuscular block [ 5 ] . CULLEN BF, STOELTINGRK, eds. Clinical anesthesia,
Similar to nonmyasthenic patients, our myasthenic patients Philadelphia: J.B. Lippincott, 1989: 441.
showed an inverse relationship between the duration of [7] OSSERMANKE. GENKINSG. Studies in myasthenia gravis:
suxamethonium block and the plasma cholinesterase review of a twenty-year experience in over 1200 patients.
Mount Sinai Journal of Medicine, New York 1971; 3 8
activity [ I I]. 497-537.
In conclusion, the present report shows that the neuro- [8] WAKID NW, TUBBEHR, BARAKAA. Assay of serum
muscular block of suxamethonium in the myasthenic cholinesterase with succinylcholine and propionylthiocholine
patient can show wide variations. Myasthenic patients may as substrates. Anesthesiology 1985; 62: 509-12.
show resistance to suxamethonium. However, the use of [9] DRACHMANDB, DE SILVAS, RAMSAYD, PESTRONKA.
Humoral pathogenesis of myasthenia gravis. Annals of the
anticholinesterase therapy with the subsequent decrease in New York Academy of Sciences 1987; 505: 90-104.
plasma cholinesterase activity can decrease the rate of [lo] CHURCHILL-DAVIDSON HC. RICHARDSON AT. Neuromuscular
hydrolysis of suxamethonium and potentiate its neuro- transmission in myasthenia gravis. Journal qf Physiology
muscular block. The degree of potentiation of blockade is 1953; 122 252-63.
[ I I] BARAKA A, WAKIDN, NOUEIHED R, KARAM H, BOLOTOVA N.
inversely related to the plasma cholinesterase activity. Pseudocholinesterase activity and atracurium v.
suxamethonium block. British Journal of Anaesthesia 1986;
58: 91s-5s.
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