Anesthetic Implications of a Near-Lethal Sodium Azide Exposure

Abstract

hour after induction of anesthesia, both RE and SE increased with respective peak values of 96 and 81. We increased the propofol and remifentanil target concentrations to values that caused hypotension, and treated him with ephedrine boluses, but this treatment failed to alter the RE and SE. The train-offour response elicited four twitches, indicating inadequate neuromuscular blockade. We treated the patient with 4 mg of cisatracurium, causing both RE and SE to abruptly decrease to 20 and 18 respectively, and BSR increased to 33 (Fig. 1).EMG artifact increased the RE and SE values, while depressing the BSR. This differs from prior reports suggesting that only RE is sensitive to EMG interference (1,2).

Sodium azide poisoning: a narrative review

“…A chemist was exposed to the equivalent of 13 g (185 mg/kg) of azide while performing an experiment using NaN 3 that led to an explosion ( Table 1(A-3) [ 39 ]). He suffered thermal and chemical burns and lacerations.…”

“…Twenty-three patients presented with hypotension [2,36,39,47,53,54,[57][58][59][60]64,73,74]. They received intravenous fluids and/or vasopressors, with some patients requiring large amounts of fluids, e.g., up to 32 L over 12 h [36].…”

Μελέτη Βιολογικών Δράσεων Νέων Μεταλλικών Συμπλόκων Του Βαναδίου Με Κυτταροτοξικές Ιδιότητες

“…Για το υδραζωτικό οξύ σε επίμυες οι τιμές LC50 και LD50 είναι αντίστοιχα 34 mg/m 3 και 33mg/kg. Το υδραζωτικό οξύ και τα αζίδια δεν έχουν υπαχθεί στην κατηγορία των μεταλλαξιογόνων και καρκινογόνων ουσιών, [Angelotti T., 2007].…”