(Acta Anaesth. Belg., 2006, 57, 157-159)
Long-lasting potentiation of a single-dose of rocuronium byamikacin : case report
V. GILLIARD (*), B. DELVAUX (**), K. RUSSELL (*) and Ph. E. DUBOIS (*)
Abstract : We report for the first time to our knowledge
tained with desflurane. She received 2 g cefazoline
long-lasting (4 hours) potentiation of single intubating
as antibioprophylaxis. Total duration was 140 min-
dose of rocuronium by a single bolus of amikacin given
utes and there was no residual neuromuscular
55 minutes later in a woman having no precipitating fac-
blockade (NMB) at the end of the procedure (train-
tor (renal failure, hepatic failure, ionic disorder, other
of-four ratio (TOF) above 0,9, ulnar nerve stimula-
drugs influencing neuromuscular function). This patient
tion at the wrist, thumb adduction measured by
had received the same rocuronium dose one month
acceleromyography ; TOF-Watch®, Organon, Oss,
sooner in similar circumstances (without aminoglycoside
The Nederlands). The patient could be then safely
antibiotic drug) and had not presented any prolongedneuromuscular blockade at this time.
Neuromuscular blockade should be monitored in every
Our patient didn’t leave hospital and had to be
patient receiving aminoglycoside antibiotic with even a
reoperated one month later because of local infec-
single intubating dose of neuromuscular blocking drug.
tion at the scar site. Before reoperation, shereceived a ten days course of amoxicilline-clavu-
Key words : Neuromuscular blockade ; rocuronium ;
lanate (2 g every 8 hours). Two days before opera-
tion serum creatinine was 1,18 mg/dl, CRP 37,GOT 76, GPT 34, gammaGT 37. Serum ions werenormal, including calcium and magnesium.
general anesthesia induced by exactly the same
drugs including 40 mg rocuronium (a single induc-
multiple drug interactions that can lead to clinically
tion bolus), and maintained by propofol (50 mg/
significant potentiation. We report a case of long-
hour) and sufentanil (5 to 10 mcg every 30-45 min-
lasting neuromuscular blockade due to synergism
utes). 55 minutes after induction of GA, patient
between a single dose of rocuronium and an
received amikacin (1 gram over 30 minutes), by
request of the surgeon. Surgery was without prob-lem. Body temperature was kept above 35,5°C. Atthe end of the procedure, 120 minutes after induc-
tion of GA, she received 2 gram of propacetamoland 100 mg of tramadol (and no NSAID), but
A 62 year old female was scheduled for a lum-
bar athrodesis. She had a Launois-Bensaude disease(subcutaneous fat deposition, thought to be genetic; can be associated to alcoholic liver disease, with
V. GILLIARD, M.D., resident in Anesthesiology ; B. DELVAUX,
megaloblastic anaemia and polyneuropathy). She
M.D., anesthesiologist, resident in Intensive Care ;
had history of hypertension, alcohol abuse but no
evidence of polyneuropathy, gastro-duodenal ulcer,
UBOIS, M.D., staff anesthesiologist.
(*) Service d’Anesthésiologie, Cliniques Universitaires de
treated asthma and obesity (90 kg, 158 cm, BMI
Mont-Godinne, Avenue G. Therasse, 1, B-5530 Yvoir,
36). No known allergy. She was taking beta-
blocker, sartan, inhaled beta-2 mimetics and corti-
(**) Acute Medicine Department, Cliniques Universitaires
Saint Luc, Avenue Hippocrate, 10, B-1200 Brussels,
costeroids, oral theophylline. Preop lab, EKG and
chest X-ray were without particularity. The proce-
Corresponding author : Philippe E. Dubois, Service
dure was performed under general anesthesia
d’Anesthésiologie, Cliniques Universitaires de Mont-Godinne, Avenue G. Therasse, 1, B-5530 Yvoir, Belgium.
induced with 200 mg propofol, 25 µg sufentanil,
Tel. : +32-81-42-39-11. Fax : +32-81-42-39-20.
45 mg ketamine, 40 mg rocuronium, and main-
E-mail : philippe.dubois@anes.ucl.ac.be. Acta Anæsthesiologica Belgica, 2006, 57, n° 2
0,6 mg/kg dose, which clinical duration is 31 minu-
muscular blockade. We had to wait 230 minutes to
tes (15-85). The drug should then have been signi-
recover the first response to TOF stimulation, and
ficantly eliminated at the time of starting amikacin,
18 more minutes to recover 4 responses but still
55 minutes later. This shows how powerful can be
with residual NMB (fading). We reversed NMB
the potentiation between these two drugs.
(2 mg neostigmine and 0,4 mg glycopyrrolate) and
Amikacin-rocuronium interactions has never
10 minutes later, TOF ratio rise above 0,9 and the
been reported to our knowledge. Although inter-
patient could be safely extubated. Blood samples
actions between aminoglycoside and neuromuscu-
taken 210 minutes after injection of rocuronium
lar blockade are known to be possible, there are
showed serum creatinine 0,8 mg/dl and serum
inconsistent. For instance, Dupuis et al found that
amikacin 88 mcg/dl. Those results were obtained
gentamycin and tobramycin prolonged the neuro-
210 minutes after initial bolus of rocuronium,
muscular actions of vecuronium but not that of
125 minutes after the end of infusion of amikacin,
atracurium (11). The long duration of NMB
and 10 minutes before observing the first response
(4 hours) after a single doses of amikacin and
rocuronium not given concomitantly, in a patientwho did not have any precipitating factors, makethis case even more interesting. Launois-Bensaude
disease doesn’t seem to be responsible of this, sinceno effect on neuromuscular junction has been
Many drugs are known to interact with neuro-
muscular blocking drugs (1). They include antibi-
Although literature shows that neostigmine
otics, inhaled anesthetics, magnesium, lithium,
produce only a partial reversal of aminoglycoside-
local anesthetics, antiepileptic drugs, some diuretics
induced block, we were able to fully reverse it with
(furosemide) and some other drugs. Some antibi-
this drug. Calcium (chloride or gluconate) has been
otics have been proved to be very safe (e.g. beta-
shown even more effective than cholinesterase
lactams) while others have proved to have neuro-
inhibitors for reversal of this type of NMB, but its
muscular properties by themselves (e.g. clin-
use is not recommended because the antagonism
damycine). Aminoglycoside can interfere with neu-
that it produces is not sustained, and it may prevent
romuscular transmission by inhibition of the cholin-
the antibacterial effect of the antibiotic (1, 2). 4-
ergic activity at a pre- and post-synaptic level (2).
aminopyridine has been used for research purpose
In experimental animal studies, amikacin has
but is not easily available for clinical use (2).
been shown to induce NMB by itself at very high
Recent data’s show that there is a high inci-
doses (80 to 200 mg/kg) (3-5) and to induce NMB
dence of residual NMB in clinical daily practice
at clinical doses (20 mg/kg) after subthreshold
until 2 hours after a single intubating dose of non-
doses of d-tubocarine (0,05 mg/kg) (3). Hashimoto
depolarinzing muscle relaxant with an intermediate
et al documented interaction of amikacin with d-
duration of action (12). Our case emphazise the
tubocarine in man, and showed significant potenti-
need to monitor every NMB, especially when
ation of NMB at low doses (200 mg), but for a short
potentiating drugs such as aminoglycoside anti-
time (a few minutes) (6). KRONENFELD et al. report-
biotics are administered concomitantly, which is
ed a recurrence of NMB after reversal of vecuroni-
frequently the case in daily practice.
um NMB, to a patient who had undergone sternalirrigation with polymyxin and amikacin (7). However polymyxin could have played an important
References
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Body Mass Index 25), our patient received a
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LONG-LASTING POTENTIATION OF A SINGLE-DOSE OF ROCURONIUM BY AMIKACIN
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of neuromuscular blockade of vecuronium in a patient
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