The Kalaemic and Neuromuscular Effects Of.2

Eur J Anaesthesiol 2015; 32:666671
ORIGINAL ARTICLE
The kalaemic and neuromuscular effects of

succinylcholine in centronuclear myopathy
A pilot investigation in a canine model
Manuel Martin-Flores, Monique D. Pare, Luis Campoy, Marta Romano, Emily A. Tomak and
Robin D. Gleed
BACKGROUND Myopathies are generally considered to
increase the risk for succinylcholine-induced hyperkalaemia
and may affect the duration of action of neuromuscular blockers. Centronuclear (myotubular) myopathy (CNM) is congenital and produces various degrees of muscular weakness and
associated complications such as respiratory failure. The
effects of succinylcholine and the potentially lethal consequences of hyperkalaemia on patients with CNM are
unknown due to its rarity. One source of information is the
dog, as CNM occurs naturally in dogs. Because of its remarkable similarity with the disease in man, canine CNM can serve
as a model to further our knowledge of the effects of succinylcholine.
OBJECTIVES We examined the kalaemic and neuromuscular effects of succinylcholine in dogs with and without autosomal-recessive CNM.
MAIN OUTCOME MEASURES Whole blood potassium

concentration was measured 5 min before and after succinylcholine administration. Neuromuscular function was
measured with acceleromyography and single twitch stimulation.
RESULTS All dogs recovered uneventfully from anaesthesia.
The increase in potassium concentration [mean (SD)] following succinylcholine was similar between groups: CNM 0.5
(0.4) mmol l1 and control 0.7 (0.4) mmol l1 (P 0.47).
Recovery of the single twitch to 25, 75 and 90% was longer
in the CNM group (all P < 0.001); 90% recovery took 35.5
(1.18) min for the CNM group and 23.3 (1.68) min for the
control group.
PATIENTS Six dogs with autosomal-recessive CNM and six

control dogs.
CONCLUSION CNM did not exacerbate the increase in

blood potassium that is ordinarily seen with succinylcholine.
Recovery from succinylcholine was nearly 50% longer in
dogs with CNM. Although our sample size is too small to
evaluate the incidence of succinylcholine-induced hyperkalaemia, extrapolation of these findings suggests that
increased duration of action should be expected if succinylcholine is given to a patient with autosomal-recessive
CNM.
INTERVENTIONS Dogs received succinylcholine 0.3 mg

kg1 during isoflurane anaesthesia.
Published online 21 January 2015
DESIGN A prospective, experimental study.

SETTING Anaesthesiology laboratory, College of Veterinary
Medicine, Cornell University, New York, USA.
Introduction
Centronuclear myopathy (CNM), also called myotubular
myopathy, is a congenital disease characterised by
centrally placed nuclei and generalised muscle weakness.1 CNM exists in X-linked recessive, autosomalrecessive and autosomal-dominant forms. The severity
of muscular weakness and associated complications such

as respiratory failure is greatest for the X-linked form and
mildest for the autosomal-dominant form.1 From observations in France, the incidence of confirmed X-linked
CNM is reported to be approximately 2/100 000 male
From the Department of Clinical Sciences, College of Veterinary Medicine (MM-F, MDP, LC, RDG), and Cornell University Hospital for Animals, College of Veterinary
Medicine, Cornell University, Ithaca, New York, USA (MR, EAT)
Correspondence to Manuel Martin-Flores, DVM, DACVAA, College of Veterinary Medicine, Cornell University, Ithaca, NY, 14853 USA
E-mail: martinflores@cornell.edu
0265-0215 Copyright 2015 European Society of Anaesthesiology. All rights reserved.
DOI:10.1097/EJA.0000000000000222
Copyright European Society of Anaesthesiology. Unauthorized reproduction of this article is prohibited.
Succinylcholine and centronuclear myopathy 667
births per year; however, the overall incidences of other

forms of CNM are unknown.1
Hyperkalaemia and even fatal rhabdomyolysis have
been associated with the use of neuromuscular blocking
agents such as succinylcholine (SCh) in patients with
other myopathies and some diseases that affect muscle
development, such as Duchenne muscular dystrophy.28
Little is known about CNM because its rarity means that
there is very little objective information available
regarding the use of neuromuscular blocking agents
in these individuals. From the available reports, it is
apparent that neuromuscular blocking agents are
usually avoided.9 11 Some anaesthesiologists have even
opted to remove SCh from the operating room when
anaesthetising patients with X-linked CNM, presumably to avoid accidental use.12 Administration of SCh to
patients with unrecognised myopathies has been
reported, in some cases with fatal results.6,13 To our
knowledge, there are no reports on the effects of SCh in
patients with CNM.
Autosomal-recessive CNM has been described in Labrador retriever dogs.14 Clinical signs and histological
characteristics of CNM in these animals are identical
to those encountered in man.15 To our knowledge, the
canine model is the only naturally occurring model available and it reflects very closely the changes that occur
with autosomal-recessive CNM in humans.15 The rarity
of CNM and the potentially lethal consequences of
hyperkalaemia exclude prospective investigations into
the use of SCh in patients, and accordingly, we have
chosen to use canine CNM as a model for a prospective
investigation into the effects of agents used during general anaesthesia in man.
In this pilot investigation, we compared the kalaemic and
neuromuscular effects of SCh in dogs with CNM against
those in control animals. We hypothesised that the
increase in blood potassium (K) after SCh administration would be greater in CNM dogs than in normal
control animals and that the duration of neuromuscular
block would be longer in the affected animals.
Materials and methods

Animals
Six purpose-bred adult Labrador retriever dogs with

diagnosed autosomal-recessive CNM, weighing 20.4 to
33.3 kg, and a group of six healthy adult purpose bred
beagles, weighing 7.1 to 11.3 kg were used. Sample size
was limited by the availability of animals with CNM.
Autosomal-recessive canine CNM was diagnosed
through DNA testing by an independent laboratory
(DDC Veterinary, Fairfield, Ohio, USA). None of the
dogs were receiving any type of medication before this
study. All procedures were approved by the Cornell
Institutional Animal Care and Use Committee (Protocol
number 2012-0088; 19 July 2012).
General anaesthesia and neuromuscular monitoring
Food but not water was withheld overnight prior to

anaesthesia. A catheter was placed in a cephalic vein
and dexmedetomidine (Dexdomitor; Orion Corporation,
Espoo, Finland) 2 mg kg1 was administered intravenously (i.v.). General anaesthesia was induced with
i.v. propofol (Propoflo; Abbott Laboratories, North Chicago, Illinois, USA) 2 mg kg1. The trachea was intubated
and the lungs were ventilated to normocapnia with isoflurane (Isothesia; Butle Schein Animal Health, Dublin,
Ohio, USA) (end-tidal concentration 1.3 to 1.5%) in
oxygen. Dexmedetomidine 2 mg kg1 h1 and lactated
Ringers solution (5 ml kg1 h1) were infused throughout the procedure. The electrocardiogram, SpO2, capnography, end-tidal isoflurane concentration, systemic
arterial blood pressure waveform and oesophageal
temperature were monitored continuously. Oesophageal
temperature was maintained between 378C and 388C by
the use of a forced warm air device.
Neuromuscular function was assessed on a thoracic limb
with acceleromyography (AMG; TOF Watch SX, Organon, Ireland) as described previously.16 Briefly, with the
dog in left lateral recumbency, the dependent limb was
held extended and slightly elevated so that the carpus
and manus (paw) could flex freely during nerve stimulation. A 150 g elastic preload was applied to the paw to
facilitate return of the carpus to an extended position
during neuromuscular monitoring. Stimulating needles
were placed subcutaneously over the ulnar nerve and the
acceleration transducer was taped to the palmar aspect of
the paw. After at least 30 min of general anaesthesia and
15 min of single twitch stimulation (0.1 Hz, pulse
duration 0.2 ms, 50 mA), the AMG monitor was calibrated
(CAL 2). Single twitch stimulation was then resumed.
After the single twitch signal had been stable for at least
3 min, SCh 0.3 mg kg1 was administered i.v. as a fast
bolus through a free-flowing infusion of the isotonic
crystalloid solution. This dose produces complete neuromuscular block in normal dogs.17,18 During recovery
from SCh, the changes in the height of the single twitch
were recorded until no further increases were observed
for at least 5 min. The average of the first six values for
single twitch amplitude after the recovery plateau was
established was used as the final single twitch amplitude.
All values for single twitch after administration of SCh
were normalised to this final single twitch value.19
Arterial blood was sampled 5 min before and 5 min after
injection of SCh for analysis of electrolytes, glucose and
acidbase status with a point-of-care device (i-STAT
system; Abbott Point of Care Inc, Princeton, New Jersey,
USA). Blood samples were obtained from the arterial
catheter and analysed immediately.
Statistical analysis
The distribution of all variables was tested for normality

(ShapiroWilk test, Minitab 16.2.4). Whole blood

668 Martin-Flores et al.
potassium concentration before and after SCh administration were compared within groups with the paired
t-test. The increase in K concentration relative to baseline was compared between groups with the two-sample
t-test. The sensitivity (gain) of the AMG monitor and all
recovery variables [return of single twitch to 25, 75 and
90% of the final single twitch height and recovery index
(interval between ST 25 and 75%)] were compared
between groups with two-sample t-tests. Differences
were considered significant when P value was less than
0.05. All parametric data are summarised as mean (SD).
Descriptive statistics [nonparametric distribution;
median (IQR)] for electrolytes other than K, acidbase
variables and glucose before and after SCh administration
are also presented.
Results
All dogs recovered uneventfully from general anaesthesia. A transient decrease in arterial blood pressure of at
least 20% was observed in two CNM dogs following SCh.
These changes were self-limiting and required no intervention.
Kalaemic, other electrolytic, acidbase and glucose

effects of succinylcholine
In two animals from the control group, venous blood

samples were used in lieu of arterial samples because of
failure of the arterial catheter. Following SCh administration, K increased by 0.5 (0.4) mmol l1 [16% (1.15)] in
the CNM group and by 0.7 (0.4) mmol l1 [18% (1.2)] in
control dogs; each was a significant increase from baseline; P 0.03 and 0.01, respectively (Fig. 1). However,
the percentage increase from baseline was not different
between groups (P 0.47). Other electrolyte, acidbase
and glucose values obtained before and after Sch administration are summarised in Table 1. There was a little
change after SCh was given.
Neuromuscular effects of succinylcholine
Onset time was 1.4 (0.4) min for CNM and 1.7 (0.6) min
for control dogs (P 0.47). Times to 25, 75 and 90%
recovery were significantly longer (P 0.001) for CNM
dogs than for controls (Fig. 2). The recovery index
was not significantly different between the treatment
groups [CNM 8.3 (3.5) vs. control 3.9 (2.1) min; P 0.15].
Performance of acceleromyography
Calibration of the AMG required several attempts in dogs

affected with CNM, in which the evoked excursion of the
paw was minimal. After calibration, the AMG reports the
value of sensitivity (gain) required to set the control
response to 100%. The sensitivity after calibration was
significantly greater for CNM dogs [CNM 481 (30) vs.
control 308 (80); P 0.003], suggesting that signal amplification by the AMG monitor was larger in those animals.
In one dog with CNM, the gain had to be increased
manually to its maximum (512) because calibration failed
after several attempts. We did not encounter any problems during AMG calibration in control animals.
In three out of six dogs with CNM, the AMG monitor
reported single twitch values between 10 and 20% at a
time when neuromuscular block was expected to be
maximal and when evoked motor response could neither
be seen nor palpated (Fig. 3). Such erroneous measurements were not observed in the control dogs (Fig. 3).
Discussion
Our results show that the increase in K after SCh was
similar for the two groups of dogs. No electrocardiographic signs consistent with hyperkalaemia, such as tall
T waves, absence of P waves or wide QRS complexes,
were observed at any time.20 In two CNM dogs, we
observed a transient decrease in arterial blood pressure
after SCh, which resolved spontaneously. This might
have been due to histamine release, but no other signs
Fig. 1
K+ (mmol L1)
Control
CNM
5.0
5.0
4.5
4.5
4.0
4.0
3.5
3.5
3.0
3.0
2.5
2.5
Pre
Post
Pre
Post
Blood potassium concentration before and after succinylcholine 0.3 mg kg1 in dogs with autosomal-recessive centronuclear myopathy and controls.
Significant increase from baseline after succinylcholine; P < 0.05. However, the increase was similar between groups.

Table 1 Median (interquartile range) concentration of electrolytes, acidbase status and glucose concentration measured 5 min before (Pre)
and 5 min after (Post) succinylcholine was given to centronuclear myopathy and control dogs
CNM
Control
Pre
pH
SBE (mmol l1)
Na (mmol l1)
iCa2 (mmol l1)
Glucose (mg dl1)
7.39
1
142.5
1.29
122
Post
(0.03)
(1.5)
(1.75)
(0.11)
(26)
7.39
0
142.5
1.3
118.5
(0.04)
(3.25)
(4.75)
(0.09)
(36)
Pre
7.3
2.5
143.5
1.38
96
(0.04)
(2)
(3.5)
(0.07)
(18.5)
Post
7.3
3
141.5
1.36
106.5
(0.02)
(2)
(5.25)
(0.03)
(11.5)
Normal
7.35 to 7.45
5 to 0
139 to 150
1.12 to 1.4
60115
iCa2, ionized calcium; CNM, centronuclear myopathy; SBE, standard base excess.
such as flushing of the mucous membranes, urticaria or

signs of bronchospasm were observed. As the highest K
concentrations recorded did not exceed the normal limit
for dogs (5.5 mmol l1), it appears unlikely that an
increase in K was responsible for these haemodynamic
changes.20 Moreover, the increment in K observed in
both groups after SCh is in agreement with previous
reports in man (0.5 to 1 mmol l1).21 In our study, K
was measured 5 min after SCh administration; we chose
5 min because in humans, the increase in K induced by
SCh peaks at 3 to 4 min.2,22,23
Succinylcholine-induced hyperkalaemia has been
reported in a variety of pathological states including
muscle trauma (inflammatory or thermal), upper and
lower motor neurone defects and severe infection,25
when SCh may be contraindicated. In patients with
disease of this nature, upregulation of extrajunctional
(fetal or immature) acetylcholine receptors and also an
isoform of the acetylcholine receptor, known as a7AChR,
is observed. Upon interaction with SCh, depolarisation of
extrajunctional and a7AChR occurs resulting in an exaggerated efflux of K.23 As we did not observe hyperkalaemia in dogs with CNM, it is unlikely that significant
upregulation of these receptors occurred. Recent observations of endplates of an individual affected with CNM
found a reduced number of acetylcholine receptors per
Fig. 2
100
CNM
Control
ST (%)
80
60
40
20
0
0
10
20
30
40
50
Time (minutes)
Spontaneous recovery of the single twitch (ST) to 25, 75 and 90%
(normalised to final single twitch value) after succinylcholine
0.3 mg kg1 in dogs with autosomal-recessive centronuclear myopathy
(CNM) and controls. Significant difference between groups; P < 0.05.
endplate and a reduction in the acetylcholine receptor

index. The authors also observed formation of immature
endplate regions that could potentially express immature
acetylcholine receptors.24
Succinylcholine is usually avoided in patients with malignant hyperthermia, as it is known to trigger the condition.
The skeletal muscle ryanodine receptor (RYR1) gene has
been implicated in the development of MH and recent
evidence has shown that RYR1 mutations can also be
involved in the development of some forms of myopathies with central nuclei or in patients presenting with
mixed diseases that include both core and central
nuclei.25,26 In at least one instance, malignant hyperthermia has developed in an anaesthetised patient with
CNM.27 Although many cases of CNM remain genetically unresolved,28 it has been suggested that RYR1
mutations might be common in individuals with CNM
and that they should be considered at risk for developing
malignant hyperthermia.26 Our experience with dogs
with autosomal-recessive CNM provided no evidence
of any signs of malignant hyperthermia being triggered
by SCh or isoflurane. Of note, this group of dogs has been
anaesthetised at least four times with isoflurane or
sevoflurane for different unrelated investigations; no
complications indicative of malignant hyperthermia were
observed.
Although there were no differences between groups in
onset time, our results show moderately longer duration
of neuromuscular blockade in dogs with CNM; the
recovery of the single twitch to 90% was delayed in
the CNM dogs by nearly 10 min. The difference in the
recovery index between groups did not quite reach
significance, but it is possible that our sample size is
too small to detect such a difference. We chose a dose of
SCh of 0.3 mg kg1 in our investigation. Although this
dose might appear lower than that typically used in
humans, in dogs, it is commonly used to produce complete block;17,18 the return of the first twitch of the TOF
to 80% of baseline after 0.3 mg kg1 SCh takes 20 to
30 min.17,18 It is possible that the longer duration of
neuromuscular block observed in the CNM dogs could
be attributed to breed differences (Labrador retriever vs.
beagle), but no breed-specific alterations in the timecourse of neuromuscular blockers have been reported for
dogs. Furthermore, when duration of SCh was compared

670 Martin-Flores et al.
Fig. 3
Control
CNM
100
ST (%)
ST (%)
100
50
50
No visible twitch
0
0
10
20
30
40
Time (minutes)
10
20
30
40
Time (minutes)
Examples of the single twitch (ST) height after succinylcholine 0.3 mg kg1 (time zero) in a control dog and one with centronuclear myopathy (CNM).
In the CNM dog, twitch heights of 20% continued to be displayed by the monitor despite the absence of any observable evoked twitch.
between greyhounds and mixed breed dogs, no differences were observed.29 It appears that the differences in
recovery times that we observed between control and
CNM dogs are relatively benign, especially if the extent
of neuromuscular blockade is being measured objectively.
Acceleromyographic monitoring in dogs with CNM
proved challenging. Several attempts were required
before calibration could be performed. This was not
the case in the control animals, nor has it been our
experience when using similar protocols in earlier work.
In one dog, calibration was not possible and the gain was
manually increased to its maximum. During calibration of
the AMG, the signal (gain) is amplified so that the
response can be set to 100%. It follows that small evoked
responses might require higher signal amplification.
When signal amplification is high, the potential for erroneous measurements arising from background noise, such
as movement from surgical table, increases. In dogs with
CNM, the sensitivity used by the AMG was significantly
higher than in the control group, indicating higher signal
amplification. In these dogs, erroneous results were
observed at the time of complete block; the AMG displayed twitch heights of up to 20% when no visible or
palpable twitch could be detected (Fig. 3). This observation suggests that AMG monitoring might be prone to
erroneous measurements whenever the evoked response is
very small (and signal amplification high), as is the case in
many patients with neuromuscular disease. Similar difficulties have been reported when calibrating an AMG
monitor on neonates and small infants and whether the
sensitivity of the AMG monitor is adequate for patients
producing small responses is in question.30 Presumably,
our experience of myopathic dogs represented an exaggeration of that observation.
Our study has limitations. The sample size is small

reflecting the availability of animals with CNM and
because this is an animal model with small numbers,
our findings cannot be extrapolated directly to humans.
Nevertheless, this study adds information that might be
relevant to anaesthesiologists presented with patients
with this rare condition. The dogs in this study were
autosomal-recessive; we cannot exclude the possibility
that autosomal-dominant individuals might behave
differently. Weakness in individuals with CNM can
worsen mildly with time.1 We cannot speculate on how
progression of the disease might affect the duration and
effects of SCh. We compared groups of dogs of different
breeds and different size and weight; the control group
was composed of beagles, which were smaller than the
Labradors with CNM. Beagles are commonly used for
research purposes, and to our knowledge, no breedrelated differences in the response to neuromuscular
blockers have been reported in dogs. We did not measure
cholinesterase activity in either group, and hence, we
cannot comment on whether that could have influenced
the duration of action of SCh. However, it is noteworthy
that duration of SCh in the beagles is in accord with
previous reports.16,17 Whole blood K concentrations
were only measured at baseline and 5 min after SCh
administration and it is possible that higher values of
K could have gone unnoticed. However, no electrocardiographic changes indicative of hyperkalaemia were
observed at any point in any of the dogs. Rhabdomyolisis
has been reported after SCh was given to patients with
other myopathies.6 Although specific biomarkers for
muscle injury were not measured in these experiments, all of the animals returned quickly to their preexperimental condition and none had signs of muscle
pain, suggesting that any muscle injury was minimal in
these animals.

In summary, SCh 0.3 mg kg1 resulted in similar onset

but longer duration of action in dogs with autosomalrecessive CNM than in control ones. Autosomal-recessive
CNM did not exacerbate the increase in K ordinarily
seen after succinylcholine in these animals. Although our
sample size is too limited to evaluate the incidence of
succinylcholine-induced hyperkalaemia, extrapolation of
these findings suggests that increased duration of action
should be expected if succinylcholine is given to a patient
with autosomal-recessive CNM.
Acknowledgements relating to this article
11
12
13
14
15
16
Assistance with the study: none.

17
Financial support and sponsorship: this work was supported by

the Section of Anesthesiology, College of Veterinary Medicine,
Cornell University.
18
Conflicts of interest: none.
19
Presentation: none.
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Eur J Anaesthesiol 2015; 32:666671