Acute and Critical Care

Case Report

Pharmacology/Anesthesiology
Lipid Emulsion in the Successful Resuscitation of Local Anesthetic Toxicity after Ankle Block: Sang Hee Park, Sang Hyun Kwak, Kyung Yeon Yoo, Hyun Jung Lee, Keun Bae Yook, Seok Jai Kim; Korean J Crit Care Med. 2014;29(3):234-236. Published online August 31, 2014; DOI: https://doi.org/10.4266/kjccm.2014.29.3.234

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Abstract PDF: Unexpected occurrence of local anesthetic toxicity is not rare and can cause fatal complications that do not respond to any known drug of intervention. Recently, the successful use of lipid emulsion for local anesthetic toxicity has been reported and recommended as a rescue method for cardiac or neurologic complications. We report a case of seizure attack and respiratory arrest successfully recovered with the use of intravenous lipid emulsion. Clinicians must be aware of the beneficial role of lipid emulsion in cases of local anesthetic toxicity.

Original Articles

Effects of Intravenous Lidocaine on Intra-abdominal Pressure during Endotracheal Suctioning: Wha Ja Kang, Seok Hee Ham, Young Kyu Choi, Moo Il Kwon; Korean J Crit Care Med. 1998;13(2):224-228.

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Abstract PDF: BACKGOUND: We evaluated the effect of intravenous lidocaine (1 mg/kg and 2 mg/kg) on intra-abdominal pressure (IAP) during endotracheal suctioning.
METHODS
We studied 40 patients undergoing endotracheal intubation during mechanical ventilation. Group I (1 mg/kg) and group II (2 mg/kg)were given lidocaine double fashion. The endotracheal suctioning (ETS) was done 1, 3, 5 and 7 min after the injection of lidocaine. IAP, systolic blood pressure (SBP), diastolic blood preassure (DBP), and heart rate (HR) during ETS were recorded, IAP was measured using a transurethral bladder catheters. The cough response to ETS was classified as " cough score".
RESULTS
Before administration of lidocaine, ETS produced significant increase in SBP, DBP, IAP and HR compared with baseline values in the two groups (p<0.05). Both groups showed no significant changes in SBP, DBP, and HR during the study. In group I, ETS produced a significant increase in IAP 5 and 7min after lidocaine treatment (p<0.05). There were significant differences between the two groups 5 and 7 min after lidocaine treatment (p<0.05). The score of cough decreased significantly in both groups 3 min after lidocaine treatment but there was a significant difference between the two groups at 7 min.
CONCLUSIONS
We concluded that lidocaine pretreatment significantly blunted the increase in IAP, SBP DBP and HR caused by ETS and this effect lasts for 3 min in group I and 7 min in group II.

The Effect of Clonidine Pretreatment on Bupivacaine-induced Cardiac Toxicity in Rabbit: Eun Ju Lee, Jin Young Chon, Yong Woo Choi, Se Ho Moon; Korean J Crit Care Med. 1998;13(2):205-211.

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Abstract PDF: BACKGOUND: Bupivacaine, an amide type local anesthetic, is frequently used for regional anesthesia. Bupivacaine overdose induces cardiac toxicity and directly depresses both cardiac electrophysiology and hemodynamic status. Clonidine, an imidazolin alpha-2-adrenoreceptor agonist, given prophylactically may delay the toxic manifestation of bupivacaine overdose and does not accentuate the subsequent hypotension. We studied the effect of clonidine pretreatment on bupivacaine induced cardiac toxicity.
METHODS
Fourteen rabbits (seven in each group) were anesthetized with ketamine and rompun, and tracheostomy was performed. Spontaneous ventilation with room air was continued throughout the experiment. Electrocardiogram, heart rate, and invasive arterial blood pressure were continuously recorded. Clonidine 5 microgram/kg (clonidine group) or saline (control group) was injected intravenously in randomized fashion. After 15 minutes, an intravenous infusion of bupivacaine was started at 0.3 mg/kg/min. The time of occurrence of the bupivacaine-induced toxic events: first dysrhythmia, 25% and 50% reduction in basal heart rate and mean arterial pressure, and asystole were recorded. At 5, 10, 15, and 20 minutes after bupivacaine infusion, 2 ml of whole blood were withdrawn via femoral arterial catheter for determination of bupivacaine concentration.
RESULTS
The threshold time at the first dysrhythmia was significantly greater in the clonidine group (27.2+/-4.5 min) than control group (19.9+/-1.2 min). The threshold times at the 25 and 50% reduction in basal heart rate were significantly greater in the clonidine group (23.7+/-5.8 min, 33.2+/-5.1 min) than control group (16.6+/-2.9 min, 22.9+/-2.8 min) and in basal mean arterial pressure were significantly greater in the clonidine group (15.6+/-2.6 min, 25.3+/-3.7 min) than control group (9.7+/-2.7 min, 16.3+/-5.8 min). The threshold time at the asystole was significantly greater in the clonidine group (38.2+/-7.7 min) than control group (28.7+/-3.4 min). At 5, 10, 15, and 20 minutes after bupivacaine infusion, there was no significant difference in the plasma bupivacaine concentration between two groups.
CONCLUSION
This study demonstrates that clonidine pretreatment delays the cardiac toxic manifestations of bupivacaine overdose. And plasma bupivacaine concentration was not influenced by clonidine pretreatment.

The Effect of Cervical Sympathetic Nerve Block on Blood-brain Barrier Disruption with Mannitol Infusion in Rats: Bong Ki Moon, Soo Han Yoon, Young Joo Lee, Chul Ryung Hur, Chang Ho Kim, Sung Jung Lee, Young Seok Lee; Korean J Crit Care Med. 1997;12(1):69-74.

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Abstract PDF: BACKGOUND: The barrier can be altered by a number of insults to the brain (e.g., hypertension, freezing, trauma, drug). But the effect of the blood brain barrier distruction immediately after the neural change is unknown. In the present study, we focused on the BBBD after cervical sympathetic chain block.
METHODS
13 male Sprague-Dawley rats were divided into 2 groups. Group 1 (N=7) was blocked with 0.5% bupivacaine on the right cervical sympathetic chain and group 2 (N=6) was blocked with 0.5% bupivacaine on the bilateral cervical sympathetic chain. All rats received 37degrees C, 25% mannitol (1.75 g/kg) via right carotid artery and then, the effect of cervical sympathetic chain block on blood-brain barrier disruption of four cerebral compartment using 99mTc-human serum albumin and Evans blue was evaluated.
RESULTS
Both groups showed blood-brain barrier disruption and there was no significant difference between group 1 and group 2 in the anterior and posterior hemisphere of the right side brain. But group 2 showed significant blood-brain barrier disruption than group 1 in anterior and posterior hemisphere of the left brain (p<0.01).
CONCLUSIONS
This results suggest that cervical sympathetic chain block can increase the degree of mannitol-induced blood-brain barrier disruption via neural arch or blood flow change.

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