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 USA Discussion Abstract References Introduction 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 O 2 flow. O 2 sat 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 locked- in 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 sensory- motor brachial plexus blockade that lasted 10 hours following resolution of the locked-in episode. “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. Case Description Images showing patient’s volar surfaces of the 2nd and 3rd digits Regional analgesia for shoulder surgery: infraclavicular block First published in: Journal of Regional Anesthesia & Pain Medicine © Jennifer N. Gentry 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. 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. 1.Stan TC, et al. Reg Anesth 1995;20: Durrani Z and Winnie AP. Anesth Analg 1991;72: Dukes RR and Alexander LA. Reg Anesth 1993;18: Mather LE, et al. Reg Anesth Pain Med 2005;30: Zink W and Graf BM. Curr Opin Anaesthesiol 2008;21:645–50. 6.Pere P, et al. Anesth Analg 2003;96:563-9.