Acute and Critical Care

Original Articles

Trauma
Comparison of ropivacaine, bupivacaine, and lignocaine in femoral nerve block to position fracture femur patients for central neuraxial blockade in Indian population: Manik Seth, Santvana Kohli, Madhu Dayal, Arin Choudhury; Acute Crit Care. 2024;39(2):275-281. Published online May 30, 2024; DOI: https://doi.org/10.4266/acc.2023.01606

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Abstract PDF: Background
Patients with a fractured femur experience intense pain during positioning for neuraxial block for definitive surgery. Femoral nerve block (FNB) is therefore often given prior to positioning for analgesia. In our study, we compare the onset and quality of block of 0.25% bupivacaine, 0.5% ropivacaine, and 1.5% lignocaine for FNB in fracture femur patients. Methods: Seventy-five adult femur fracture patients were equally and randomly divided into three groups to receive 15 ml of either 0.25% bupivacaine (group B), 0.5% ropivacaine (group R), or 1.5% lignocaine (group L) for FNB prior to positioning for neuraxial blockade. Onset and quality of block were assessed, as well as improvement in visual analog scale (VAS) score, ease of positioning, and patient satisfaction. Results: Percentage decrease in VAS was found to be highest in group R (82.8%) followed by groups L and B. Time to achieve a VAS of less than 4 was found to be 26.2±2.4 minutes in group B, 8.5±1.9 minutes in group R, and 4.1±0.7 minutes in group L (P<0.001). In group B, 12 patients required additional fentanyl to achieve a VAS <4. Patient positioning was reported to be satisfactory in all patients in group R and L, while in B it was satisfactory in 13 (52%) patients only. Patient acceptance of FNB was 100% in group R and L, but only 64% in group B. Conclusions: Based on our findings, 0.5% ropivacaine is a favorable choice for FNB due to early onset, ability to yield a good quality block, and good safety profile.

Hemodynamic Comparison between Bupivacaine and Levobupivacaine Induced Cardiovascular Collapses in Anesthetized Dogs: Chul Woo Jung, Jin Tae Kim, Yun Suk Choe, Seng Sim Bae, Jie Ae Kim, Hyun Sung Cho, Kook Hyon Lee; Korean J Crit Care Med. 2004;19(2):86-97.

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Abstract PDF: BACKGROUND
Levobupivacaine is known to be less cardiotoxic than racemic bupivacaine but some authors have reported there were no differences in cardiotoxic profiles between two agents. We will investigate the full course to cardiovascular collapse induced by bupivacaine stereoisomers in anesthetized dogs and would find out the differences if any, and explain the causative factors. METHODS: Twenty dogs were assigned to two groups, racemic bupivacaine group (BUP) and levobupivacaine group (LBUP), equally (n=10, each). Under general anesthesia each drug was infused continuously (0.5 mg/kg/min) until cardiovascuar collapse (CVC, MAP=40 mmHg) occurred. During the experiment, hemodynamic data, CO, SVR, PVR, ECG parameters and drug concen tration were gathered and analyzed. RESULTS: Two groups were not different in terms of dose for CVC, plasma drug concentration and time for CVC. MAP maintained initial values during the early period and declined during the late period without any between-group difference. Otherwise CO decreased continuously and significantly higher in LBUP than in BUP throughout. Calculated SVR showed the same feature as CO in opposite direction and was higher in BUP. Correlation test revealed high correlation between CONC and SVR or PVR and between CO and cSvO2. CONCLUSIONS: In assessment of cardiovascular collapse induced by stereoisomers of bupivacaine, monitoring with only MAP can lead to misinterpretation and invasive monitoring including CO or cSvO2 measurement might be needed.

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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