A Case of Reversible Locked-In Syndrome Due to
Unintentional Intravascular Injection Following
Trans-Arterial Brachial Plexus Block
Gregory N. Kozlov, DO, Maunak V. Rana, MD and Kenneth D. Candido, MD
Department of Anesthesiology, Advocate Illinois Masonic Medical Center, Chicago, IL 60657 USA
Abstract
Case Description
Discussion
Trans-arterial axillary brachial plexus block (TAAB)
is a simple upper extremity block which provides
anesthesia and analgesia for painful states and an
increase in blood flow when desirable.
Complications include
neuropathy, myalgias,
arterial spasm, hematoma, and low incidence
unintentional intravascular injection (0.2%).1
We present a case of transient “locked-in
syndrome” in a 51 yo African American renal failure
patient likely related to unintentional intravascular
injection of local anesthetic in a patient undergoing
a series of upper extremity blocks to treat ischemic
pain secondary to peripheral vascular disease.
This case is unique in that the patient, theoretically,
would have experienced delayed onset of central
nervous system toxicity due to elevated alpha-1
acid glycoprotein levels, however, CNS toxicity
became apparent within one minute of injection.
A 51yo, man presented to the Pain Clinic complaining of necrosis and pain in the right distal 2nd
and 3rd digits for the preceding 4wk. The pain was spontaneous and associated with swelling
and volar skin breakdown. The patient denied fever, chills, infection, or trauma. Past medical
history was notable for ESRD, HTN, and DM2. The patient began a weekly series of
infraclavicular (ICNB) alternating with axillary brachial plexus blocks (TAAB).
After obtaining consent, the patient was placed on the examination table in the supine position. A
20ga IV was placed prophylactically. Blood pressure, EKG, and pulse ox were monitored; after
noting stable vitals, the patient received either an ICNB or a TAAB. The ICNB were performed
with the aid of peripheral nerve stimulation. At the time of each block, 35-40mL of 0.5%
ropivicaine was injected incrementally, with intermittent aspiration to check for intravascular
needle position. At the time of the 8th TAAB, 1 minute after completing a 35mL injection, the
patient became somnolent and unresponsive. Previously, he was answering questions
appropriately. He then, with eyes-wide-open, became non-communicative and unresponsive to
verbal stimuli. His mouth opened, he did not seize or shake. Oxygen saturation remained > 95%
on room air. BP was in the 190s/90s (at the pre-procedure range); and the respiratory rate was
undetectable. The patient was immediately resuscitated with a nasal trumpet with 6L/min O2 flow.
O2sat increased to 100%. Pharmacological intervention was deemed unnecessary, as the
placement of the trumpet stimulated spontaneous respiration. The episode lasted less than 5
minutes, with the patient fully recovering from his catatonic-like state. He stated that he was able
to hear our questions during the episode and he was acutely aware of his surroundings, but he
was not able to move or respond. He stated he felt “trapped” in his body.
Common causes of the “Locked-In Syndrome” include
vertebral/basilar artery spasm, lower pontine damage, trauma,
stroke, and rarely intravascular injection of local anesthetics.
Ropivacaine is metabolized in the liver with subsequent renal
excretion. Free ropivacaine exerts its clinical effect by binding
plasma protein Alpha-1 acid glycoprotein (AAG). The
recommended maximum dose of ropivacaine is 225mg.4,5
This case involved the administration of 175 mg of 0.5%
ropivacaine, injected in a trans-arterial axillary block technique;
because the axillary brachial plexus elements are anatomically
distant from the epidural and subarachnoid spaces, locked-in
syndrome is the most likely diagnosis.
However, certain confounding factors exist with this case: the
onset of locked-in syndrome, the duration of the episode, and the
patient presentation. The patient developed symptoms of lockedin syndrome one minute after injection. Given the patient’s history
of chronic renal failure, the patient would have a relatively greater
AAG level,6 resulting in less free ropivacaine. Theoretically, this
increased AAG level would serve a protective function by buffering
against acute central nervous system toxicity and delaying the
onset of a reaction to local anesthetic injection.
Furthermore, the duration of the event is not readily explained
given the patient’s underlying medical conditions. Five minutes
after the unresponsiveness developed, the patient spontaneously
regained complete motor and mental function. Given the intrinsic
vasomotor property of ropivacaine, it would follow that CNS toxicity
would be prolonged as toxic levels of local anesthetic would be
reached 16 minutes after injection; AAG may have acted as a
buffer to the duration of toxicity. Despite having signs consistent
with locked-in syndrome, this patient experienced a solid sensorymotor brachial plexus blockade that lasted 10 hours following
resolution of the locked-in episode.
Introduction
•“Locked-In Syndrome” describes a quadriplegia
of voluntary muscles with the exception of the
ocular muscles, presenting with the patient being
fully aware of their surroundings despite being
unable to verbally communicate. 2,3
• The presence of short term paralysis and apnea
along with hemodynamic stability, leads to a
diagnosis of a reversible locked-in syndrome.
• This has been known to result following systemic
absorption of local anesthetic; however, these
cases were associated with seizure activity.
• Our case is unique in that the patient exhibited
widening of the eyes with development of a
subsequent transient yet unresponsive state,
characterized as being aware of his surroundings
and having fully intact 8th cranial nerve function.
The patient had no residual sequelae during
monitoring for 1 hour. He refused further
evaluation.
During follow-up visits, he
underwent subsequent blocks without any
complications.
Images showing patient’s volar surfaces of the 2nd and 3rd digits
References
Regional analgesia for shoulder surgery:
infraclavicular block
First published in: Journal of Regional
Anesthesia & Pain Medicine
© Jennifer N. Gentry
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