Polymyoclonus Seizure

Resulting from
Accidental
Injection of Tranexamic
Acid in Spinal
Anesthesia

Anesth Analg Vol. 108,

 We present a case of accidental injection of
tranexamic acid instead of bupivacaine during
spinal anesthesia. One minute after
intrathecal injection of 3.5 mL of solution, the
patient developed myoclonus of his lower
extremities. Accidental intrathecal injection of
the wrong drug was suspected and a used
ampule of tranexamic acid discovered in the
trash can. The ampules of tranexamic acid
(500 mg/5 mL) and bupivacaine (5
mg/mL) were similar in appearance.
General anesthesia was induced. Ten hours
later, the patient developed myoclonus of his
.
upper extremities and face. His
polymyoclonus was successfully treated with
phenytoin, sodium thiopental infusion, sodium
 CASE DESCRIPTION
A 57-yr-old man, presented for orthopedic
surgery under spinal anesthesia after left
patellar fracture. He had no remarkable
medical history except for smoking (20
packs/year) and opioid addiction (opium
smoking about 9 g/d) for 7–8 yr. Physical
examination and laboratory investigation
revealed no abnormal findings. His arterial
blood pressure was 130/80 mm Hg,
preoperatively. Spinal anesthesia was
performed with the patient in the sitting
About 30 s after injection of 3.5 mL of 0.5%
bupivacaine, the patient complained of
perianal burning. The pain in the fracture site
subsided.
However, after about 1 min, the patient’s
arterial blood pressure increased to 165/95
mm Hg and myoclonic movements developed
in the lower extremities. IV sedation with
midazolam (2 mg) and fentanyl
(100microgram) was administered
immediately without effect.
Consequently, general anesthesia was
induced by the infusion of propofol (120 mg)
and atracurium (40 mg), and the patient’s
trachea was intubated.
Accidental intrathecal injection of the wrong
drug was
suspected and a used ampule of tranexamic
acid was found
in the trash can.
The ampules of tranexamic acid (500 mg/5 mL,
Caspian Tamin Pharmaceutical Co, Rasht, Iran)
and bupivacaine (5 mg/mL, Merck, Darmstadt,
Figure 1.

Similar
appearance of
tranexamic acid
(Caspian Tamin
Pharmaceutical
Co, Rasht, Iran)
and bupivacaine
(Merck,
Darmstadt,
Germany)
ampules led to a
spinal
Propofol infusion was discontinued 1.5 h
postoperatively,
and the muscle relaxant was reversed with
neostigmine
(0.06 mg/kg) and atropine (0.02 mg/kg).
However, 1 min thereafter, myoclonic
movements recurred in a more severe form.
Therefore, atracurium (20 mg) was
administered again, together with IV diazepam
(10 mg) and dexamethasone (8 mg). Propofol
infusion (50microgram/kg/min) was also
recommenced.
After consulting with a neurologist, IV
phenytoin (500 mg initial dose, followed by
The patient was transferred to the intensive
care unit about 2 h after the injection and
mechanical ventilation with synchronous
intermittent mandatory ventilation mode was
established.
A Foley urethral catheter, nasogastric tube and
central venous and arterial lines were inserted.
The first postoperative arterial blood gas
analysis revealed metabolic acidosis (pH
=7.07, Paco2= 36.5, PaO2= 134, HCO3= 10.4,
Base Excess= -18.8, Spo2= %96). Therefore,
7.5% sodium bicarbonate (150 mL) was
infused over a period of 45 min.
Arterial blood gas analysis 2 h later revealed
The patient’s arterial blood pressure
decreased after the control of acidosis (95/65
mm Hg) without signs of hypovolemia, and
dopamine infusion (5–10 microgram/kg/min)
was initiated.
Hepatic, renal, and hematological evaluations
were done for assessing multiorgan failure.
Central venous pressure remained between 8
and 10 cm H2O.
Urinalysis showed ketone body , protein , HB,
The patient experienced a tonic clonic
convulsion in the upper extremities and the
face 10 h postoperatively, which was treated
by an infusion of sodium thiopental (3–5
mg/kg/h).
Gastric lavage of sodium valproate tablets (200
mg thrice daily) was started (the injection form
of sodium valproate was not available) to
control polymyoclonus after 24 h. The
phenytoin was tapered to 50 mg twice a day
and then discontinued after 24 h.
Thiopental was also tapered on the second
postoperative day.
On the third postoperative day, the patient’s
level of consciousness increased. He moved his
head and upper extremities with painful
stimulus, but deep tendon reflexes were
absent in the lower extremities. His arterial
On the fourth postoperative day, he opened his
eyes to voice commands, obeyed simple
orders, and was tracheally extubated. Deep
tendon reflexes were normal and his arterial
blood pressure was now 120/80 mm Hg;
therefore, dopamine was discontinued.
On the fifth postoperative day, he spoke
normally. However, strength of the right leg
was weaker than the left (3/5 vs. 4/5).
Finally, on the sixth postoperative day, all
neurologic examinations were normal,
including strength of the lower extremities
(5/5). He did not remember postoperative
events.
On the seventh postoperative day, the patient
was discharged form the intensive care unit
and on the eighth day was subsequently
 DISCUSSION
Some factors that have been identified as
contributing to medication errors include
labels, appearance and location of
ampules and syringes, inattention, poor
communication, carelessness, and
fatigue on the part of the
anesthesiologist. In this case report, drug
error-induced polymyoclonus occurred from
injecting tranexamic acid for spinal
anesthesia due to confusing two different
ampules with similar appearance. This
Myoclonus could arise from the
Cerebral cortex
Brainstem
Spinal cord
Peripheral nerves plexus, and
Spinal roots
Some authors have linked it to
cerebellar dysfunction
There are two clinical types of myoclonus
arising from the spinal cord:
Spinal segmental myoclonus and
Propriospinal myoclonus.
In the second type, the first muscles activated
are usually from the thoracic cord with
upward and downward spread resulting in
generalized myoclonus. Most patients with
propriospinal myoclonus have had minor
spinal trauma with normal magnetic
resonance imaging findings, but the disorder
has been reported in severe spinal cord injury,
multiple sclerosis, human immunodeficiency
virus or lyme infection, syringomyelia, spinal
Volumes of local anesthetics injected in the
subarachnoid space in the lumbar area can
reach the dependent structures in the
cranium, such as the cerebellum and lower
cranial nerves.
Dreskin et al. reported a case of
polymyoclonus resulting from accidental
subarachnoid injection of a local anesthetic.
Because of the dependent anatomical position
of the cerebellum and its frequent association
with myoclonus, they concluded that a local
anesthetic, steroid, or preservative effect on
the cerebellum was the most likely cause of
the patient’s polymyoclonus . In this setting,
polymyoclonus can also represent lidocaine -,
Spinal myoclonus has been described by
Brown et al. in patients after spinal cord
trauma and subarachnoid injections of
irritating substances during myelography.

Manconi et al. reported a severe and

uncommon case of propriospinal myoclonus
that appeared after a vertebral fracture of T11
vertebra and an acute progression into a
myoclonic status associated with respiratory
failure and loss of consciousness.

Some authors believe that the action of local

anesthetic drugs and IV anesthetics, such as
etomidate on the spinal cord and/or
Ford et al. reported a case of spinal myoclonus
induced by the tip of an intrathecal catheter in a
35-yr-old patient. The myoclonus resolved
promptly once the catheter tip was withdrawn.
In the present case, we observed polymyoclonus
as propriospinal clonus resulting from spinal cord
and possibly brainstem irritation by tranexamic
acid, leading to polymyoclonus and seizure.
Phenytoin did not terminate such severe
contracting movements and myoclonic seizures,
but the addition of sodium valproate was
effective.
Paralysis does not allow for evaluation of
continuing myoclonus and seizure activity but
may reduce the metabolic requirements.
Although clinical features are important,
neurophysiologic studies provide the most
important clues for the determination of the
myoclonus generator.
Surface electromyography suggests either a
cortical, brainstem or spinal origin.
Electroencephalography-electromyography
polygraphy is the only test which is able to
directly prove the cortical origin of myoclonus.
Thank you