Case Report Intraoperatively Diagnosed Tracheal Tear after Using an NIM EMG ETT with Previously Undiagnosed Tracheomalacia

Tracheal rupture is a rare complication of endotracheal intubation. We present a case of tracheal rupture that was diagnosed intraoperatively after the use of an NIM EMG endotracheal tube. A 66-year-old female with a recurrent multinodular goiter was scheduled for total thyroidectomy. Induction of anesthesia was uncomplicated. Intubation was atraumatic using a 6 mm NIM EMG endotracheal tube (ETT). Approximately 90 minutes into the surgery, a tracheal tear was suspected. After confirming the diagnosis, conservative treatment with antibiotic coverage was favored. The patient made a full recovery with no complications. Diagnosis of the tracheal tear was made intraoperatively, prompting early management

Propofol induces MAPK/ERK cascade dependant expression of cFos and Egr-1 in rat hippocampal slices

Background: Propofol is a commonly used intravenous anesthetic agent, which produce rapid induction of and recovery from general anesthesia. Numerous clinical studies reported that propofol can potentially cause amnesia and memory loss in human subjects. The underlying mechanism for this memory loss is unclear but may potentially be related to the induction of memory-associated genes such as c-Fos and Egr-1 by propofol. This study explored the effects of propofol on c-Fos and Egr-1 expression in rat hippocampal slices. Findings: Hippocampal brain slices were exposed to varying concentrations of propofol at multiple time intervals. The transcription of the immediate early genes, c-Fos and Egr-1, was quantified using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). MAPK/ERK inhibitors were used to investigate the mechanism of action. We demonstrate that propofol induced the expression of c-Fos and Egr-1 within 30 and 60 min of exposure time. At 16.8 μM concentration, propofol induced a 110% increase in c-Fos transcription and 90% decrease in the transcription of Egr-1. However, at concentrations above 100 μM, propofol failed to induce expression of c-Fos but did completely inhibit the transcription of Egr-1. Propofol-induced c-Fos and Egr-1 transcription was abolished by inhibitors of RAS, RAF, MEK, ERK and p38-MAPK in the MAPK/ERK cascade. Conclusions: Our study shows that clinically relevant concentrations of propofol induce c-Fos and down regulated Egr-1 expression via an MAPK/ERK mediated pathway. We demonstrated that propofol induces a time and dose dependant transcription of IEGs c-Fos and Egr-1 in rat hippocampal slices. We further demonstrate for the first time that propofol induced IEG expression was mediated via a MAPK/ERK dependant pathway. These novel findings provide a new avenue to investigate transcription-dependant mechanisms and suggest a parallel pathway of action with an unclear role in the activity of general anesthetics

Pulseless electrical activity during electroconvulsive therapy: a case report

Abstract Background Arrhythmias resulting in cardiac arrest during electroconvulsive therapy have been reported. Most reported cases of cardiac arrest had asystole as the initial rhythm. Pulseless electrical activity as an initial rhythm of cardiac arrest during electroconvulsive therapy has never been reported. Also, thromboembolism after inflation of pneumatic tourniquet during lower limb surgery has been reported but never following tourniquet inflation during an electroconvulsive therapy. Case presentation We report a case involving an 81- year- old female who presented to us for an electroconvulsive therapy for severe depression and developed pulseless electrical activity immediately after electroconvulsive therapy. She was successfully resuscitated and was later found to have bilateral pulmonary emboli with a complete occlusion of the right lower lobe pulmonary artery. The source of embolus was from her left lower extremity deep venous thrombus, which we believe, got dislodged intraoperatively after inflation of pneumatic tourniquet. Our patient not only survived the massive pulmonary embolus, but also showed significant improvement in her mental status compared to her pre-admission level at the time of discharge to a sub-acute rehabilitation centre. Conclusion We recommend that patients who are elderly and at high risk of thromboembolism should selectively undergo a preoperative doppler ultrasound for deep venous thrombosis. Also, selective application of tourniquet in the upper limb, to monitor for seizure activity, would reduce the incidence of pulmonary thrombo-embolism as embolic events are significantly less from deep venous thromboses of upper extremities when compared to lower extremities.</p

Bicarbonate plus epinephrine shortens the onset and prolongs the duration of sciatic block using chloroprocaine followed by bupivacaine in sprague-dawley rats.

BACKGROUND: Chloroprocaine is a fast-acting local anesthetic, whereas bupivacaine is a long-acting one. They have been coadministered with limited success. The objective of this study was to determine the effect of additives on the efficacy of regional blockade using chloroprocaine followed by bupivacaine. METHODS: Four groups of Sprague-Dawley rats, 20 each, were administered chloroprocaine followed by bupivacaine to induce sciatic nerve blockade. Group 1 received chloroprocaine with isotonic sodium chloride solution followed by bupivacaine and was used as a control. Group 2 received chloroprocaine with isotonic sodium chloride solution and epinephrine followed by bupivacaine with epinephrine. Group 3 received chloroprocaine with sodium bicarbonate followed by bupivacaine, and group 4 received chloroprocaine with sodium bicarbonate and epinephrine followed by bupivacaine with epinephrine. The time to onset and duration of anesthesia were measured for all 4 groups. RESULTS: The block using chloroprocaine followed by bupivacaine in group 1 had an onset of 2.5 mins (SD, 0.4 mins) and duration of 104 mins (SD, 16 mins). Adding epinephrine to both chloroprocaine and bupivacaine (group 2) did not significantly change the onset (2.8 mins [SD, 1.3 mins]; P = 0.35) or duration (110 mins [SD, 25 mins]; P = 0.23). With group 3, adding bicarbonate to chloroprocaine hastened the onset (1.2 mins [SD, 0.4 mins]; P \u3c 0.0001) and shortened the duration (87 mins [SD, 13 mins]; P = 0.008). In group 4, adding bicarbonate and epinephrine to chloroprocaine and epinephrine to bupivacaine hastened the onset (1.4 mins [SD, 0.4 mins]; P \u3c 0.0001) and increased the duration (130 mins [SD, 23 mins]; P \u3c 0.0001). CONCLUSIONS: Sodium bicarbonate plus epinephrine shortens the onset and prolongs the duration of a chloroprocaine-bupivacaine sciatic block in Sprague-Dawley rats