Acute and Critical Care

Case Reports

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.

Vagal Reflex Induced Bronchospasm: Tae Hyeong Kim, Yong Lak Kim; Korean J Crit Care Med. 2000;15(2):113-116.

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Abstract PDF: The parasympathetic nervous system has been considered to have an important role in bronchospasm. Although vagal reflexes are well documented in animal models of airway hyperresponsiveness, their importance in asthmatic attacks in man is less documented. We report a case of bronchospasm during sclera buckling operation and we believe that this patient's bronchospasm was induced by the vagal reflex.

Continuous Infusion of Ketamine in Mechanically Ventilated Patient in Septic Shock with Status Asthmaticus: Bon Nyeo Koo, Shin Ok Koh, Sung Yong Park, Jae Kwang Shim, Sung Sik Chon; Korean J Crit Care Med. 2000;15(2):108-112.

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Abstract PDF: Ketamine is well known for its analgesic, bronchodilating and sympathetic stimulating effect. Hence, it has been widely used for induction of patients with hypotension or asthma and also for analgesic and sedating purposes in the ICU. We presented a 62 year old female patient with ventilator support in septic shock with refractory asthma whom we managed successfully with continuous intravenous infusion of ketamine postoperatively in the ICU. The patient had a history of asthma but had been asymptomatic recently and was scheduled for an emergent explo-laparotomy under the diagnosis of acute panperitonitis. Before the induction of anesthesia, the patient was in septic shock but no wheezing could be auscultated. After the induction of general anesthesia and endotracheal intubation, wheezing was apparent in both lung fields with a high peak inspiratory pressure. Inotropics, vasopressors and bronchodilators were promptly instituted without any improvement of asthma and the patient had to be transferred to the ICU with intubated after the operation. Clinical symptoms of asthma continued throughout the first day despite using bronchodilators under mechanical ventilation but, after starting the IV infusion of ketamine, there were decrease in the peak inspiratory pressure and wheezing with a subsequent improvement in the arterial blood gas analysis findings. We could also achieve considerable analgesic and sedating effect without any decrease in the blood pressure. The patient's general physical status improved and weaning with extubation was successfully done on the 21st day and was transferred to the general ward on the 28th day.

The Use of Thiopental Sodium with BIS Monitoring in Hypoxic Brain Damage: Jae Young Kwon, Sul Ki Song, Kyung Hoon Kim, Sang Wook Shin, Seong Wan Baik; Korean J Crit Care Med. 2000;15(1):52-55.

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Abstract PDF: Hypoxemia is a common and potentially serious postoperative complication. Hypoxic encephalopahty may occur in prolonged hypoxemia. This condition needs brain protection. There are many brain protective methods. The primary cental nervous system protective mechanism of the barbiturates is attributed to their ability to decrease the cerebral metabolic rate, thus improving the ratio of oxygen (O2) supply to O2 demand. The electroencephalogram-derived bispectral index system (BIS) is a promising new method to predict probability of recovery of consciousness. We experienced two cases of hypoxic brain damage in recovery room. The patients were treated with thiopental and monitored with BIS. The use of thiopental as brain protection during complete global ischemia after cardiac arrest was not effective.

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.

Clinical Study of Diffusion Hypoxia in Early Period after Nitrous Oxide Anesthesia: Hae Keum Kil, Won Oak Kim, Sung Jin Lee, Woo Kyung Lee; Korean J Crit Care Med. 1998;13(1):55-60.

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Abstract PDF: Introduction: Anesthesiologists have been aware of the dangers of diffusion hypoxia in the early postoperative period after nitrous oxide anesthesia, but it was suggested of a little clinical significance in healthy patients. Goal of this study is to re-evaluate the possibility of diffusion hypoxia.
METHODS
Eighty patients who were scheduled for vitrectomy were allocated to two groups by normal and abnormal chest X-ray findings and each group was divided into two subgroups by N2O concentration (1-a, 2-a; 50%, 1-b, 2-b; 60%). One and half hours after anesthesia, end-tidal alveolar concentration of oxygen (et-O2), N2O (et-N2O), and PaO2 were measured for 10 minutes after the inspired gases were changed to room air 2 L/minute with controlled ventilation in group 1-a. Those parameters were re-measured after re-administration of O2 and N2O of 50% of each for an hour and the inpired gases were changed to room air again.
RESULTS
In group 1-a, there was no significant differences of et-N2O and PaO2 after 5 minutes by air flow. And there was no differences of et-N2O and PaO2 between group 1-a and 1-b by et-N2O after 4 minutes. In group 1-b, PaO2 was in normal range at 10 minutes after, although et-O2 was decreased to 14.9%. However, group 2-b showed peripheral arterial saturation lower than 96% after 6 minutes and mild hypoxemia (PaO2 75.3 mmHg) at 10 minutes.
CONCLUSIONS
We suggest that hypoxemic episode during spontaneous breathing of room air in early postoperative period after nitrous oxide anesthesia may be occur due to decreased ventilatory function rather than diffusion of nitrous oxide. However, in patients with minimal abnormal chest X-ray findings even without clinical symptoms, it would be better to avoid high concentration of nitrous oxide.

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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