Acute and Critical Care

Case Reports

Toxicology
Acute Colchicine Poisoning Treated with Granulocyte Colony Stimulating Factor and Transfusion: Sung-Hwa Lee, Sung-Wook Park, Sang-Kyoon Han, Soon-Chang Park; Korean J Crit Care Med. 2015;30(3):207-211. Published online August 31, 2015; DOI: https://doi.org/10.4266/kjccm.2015.30.3.207

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Colchicine poisoning is rare but can cause potentially life-threatening toxic complications such as hypovolemic shock, cardiovascular collapse and multiple organ failure. In this case report, we describe a case of a 20-year-old female who presented to the emergency department after suicidal ingestion of a toxic dose of colchicine. She developed thrombocytopenia, neutropenia and acute respiratory distress syndrome that required blood transfusion and administration of granulocyte colony stimulating factor for the prevention of infectious complications. With regard to the clinical manifestations of colchicine toxicity, we discussed suggested mechanisms.

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Severe colchicine poisoning treated successfully with kidney replacement therapy and plasmapheresis: a case report
D. H. Schaffer, D. L. Overbeek, T. B. Erickson, E. W. Boyer, C. Goldfine, S. A. Muhsin, P. R. Chai
Toxicology Communications.2022; 6(1): 46. CrossRef

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.

Amiodarone-induced Pulmonary Toxicity within a Short Period of the Initiation of Amiodarone Therapy: A Case Report: Woo Jin Jang, Hae Ri Chon, Jin Sung Jung, Seung Hyun Yoo, Kyu Han Koh, Young Min Koh, Jung Hyuk Kim; Korean J Crit Care Med. 2011;26(2):117-121.; DOI: https://doi.org/10.4266/kjccm.2011.26.2.117

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Amiodarone is one of the most commonly prescribed antiarrhythmic drug for almost all atrial or ventricular arrythmias. Amiodarone-induced pulmonary toxicity (APT) was first described in 1980 and has potentially serious side effects that are believed to develop in 5% of patients. In general, APT occurs only when high amiodarone doses are used for a long time. However, during short-term therapy of amiodarone, APT is rarely reported. In this report, we describe a case of amiodarone-induced pulmonary toxicity after a short course of amiodarone therapy for atrial fibrillation.

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A Case of Acute Hepatitis Associated with Intravenous Infusion Amiodarone in Patient with Atrial Fibrillation
Ji Hye Lee, Myug-Shin Kang, Tae-Hoon Kim, Dong Hee Shin, Rak Kyeong Choi, Su Jin Jung
Soonchunhyang Medical Science.2015; 21(2): 208. CrossRef
Amiodarone Induced Multiorgan Toxicity in a Patient of Hypertrophic Cardiomyopathy With Atrial Fibrillation
Dae Jung Kim, Sang Chil Lee, Gi Soo Park, Gyung Jung Kim, Won Tae Hwang, Chang Soo Lee, Moo Hyun Lee, Dae Hee Hahn, Hyeon Cheol Koh
Journal of the Korean Geriatrics Society.2013; 17(4): 223. CrossRef
Very Early Onset of Amiodarone-Induced Pulmonary Toxicity
Wonho Lee, Dong Rueol Ryu, Seon-Sook Han, Sook-Won Ryu, Byung Ryul Cho, Hyucki Kwon, Bo Ra Kim
Korean Circulation Journal.2013; 43(10): 699. CrossRef
Amiodarone-Induced Pulmonary Toxicity: Percutaneous Needle Aspiration Biopsy and Ultrastructural Findings
In Sook Kang, Jin Hwa Lee, Sun Hee Sung, Seong Hoon Park
The Ewha Medical Journal.2013; 36(2): 144. CrossRef

Original Articles

The Effects of Chemotherapeutic Agents on Renal Function during Continuous Hyperthermic Peritoneal Perfusion: Jong Ho Choi, Eun Sung Kim; Korean J Crit Care Med. 2002;17(1):19-24.

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Abstract PDF: BACKGROUND
Continuous hyperthermic peritoneal perfusion (CHPP) has been introduced to improve the survival of the advanced cancer patients. It is a technique that allows uniform delivery of cytotoxic agents and heat to the peritoneal surface. However CHPP - induced acute changes of body temperature and intraabdominal pressure could produce various abnormal physiologic responses, especially hypoperfusion and hypoxia. These factors may further contribute to the renal dysfunction. Moreover, transperitoneal absorption of drugs resulting in systemic toxicity and certain anticancer drugs have an inherent nephrotoxicity. The aim of the present study was to investigate the effect of anticancer drugs on the kidney in the ovarian cancer patients after CHPP.
METHODS
CHPP with anticancer agents in warm saline was performed in 54 patients with cancer of the ovary at temperature 47 degrees C for 90 minutes under general anesthesia. Forty nine patients were given carboplatin and 5 patients were received cisplatin intraperitoneally at an equi-toxic dose. To clarify the effect of cisplatin and carboplatin on the kidney, serum creatinine and blood urea nitrogen (BUN) were measured before anesthesia, 1, 3 and 7th day after surgery in both agents.
RESULTS
There were no significant changes of creatinine level on 1, 3 and 7 days postoperatively compared to preoperative creatinine in carboplatin patients. In carboplatin patients, postoperative BUN levels were decreased significantly on 1 and 3 days, but they were within normal range. BUN level of postoperative 7 day showed no significant change. In cisplatin patient, there was insignificant increase of BUN and creatinine levels on 1, 3 and 7 days postoperatively.
CONCLUSIONS
These results suggest that carboplatin did not suppress renal function until 7 days after CHPP. Cisplatin markedly increased the creatinine and BUN until 7 days postoperatively, but there was no statistical significance.

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.

Endobronchial Insufflation of Air Supports Ventilation in Apneic Dogs: Ji Han Rhyu, Sun Gyoo Park; Korean J Crit Care Med. 1998;13(2):198-204.

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Abstract PDF: BACKGOUND: Mass casualties from organophosphorus inhalation die from respiratory depression. Gas supplies and equipment are limited for mechanical ventilation of multiple subjects in emergency situation. Endobronchial insufflation of air (EIA) can be simply performed with air compressor and catheter. The author tried to examine the usefulness of EIA in five apneic dogs induced by tetrodotoxin (TTX) infusion.
METHOD
Five anesthetized dogs were intubated with endotracheal tube and endobronchial insufflation catheter and instrumented with arterial catheter and ventilated with controlled mechanical ventilation (CMV) while 12 microgram/kg TTX was infused intravenous over 90 minutes to produce apnea. EIA of 1 microliter/kg/min was delivered through a 35 cm long, 0.8 cm ID catheter with a forked end placed astride the carina. During conventional ventilation, arterial blood gases and pH were measured (base line, BL). The data were measured after confirmation of apnea for 1 minute (time=0, control value), and then measured serially for 4 hours of EIA.
RESULT
All animals survived and were alert and neurologically normal within 24 hours. The changes of arterial oxygen tension (PaO2) were no significant difference between control value and 10, 20, 30 minute (p<0.05), and arterial carbon dioxide tension (PaCO2) were significant increase in control value compared to base line (p<0.05), and pH were no significant difference in all values (p<0.05). Spontaneous respiratory efforts slowly returned after 45 minute of EIA and resulted in the improvement of gas exchange.
CONCLUSION
EIA recognized as a sort of ventilatory technique is useful only when other equipments could not be available. The EIA catheter can be placed by cricothyroidotomy. EIA is very helpful in supporting ventilation, and it also helps the apneic dogs stay in normal condition.

The Effects of Repeated Toluene Exposure on Amino Acid Neurotransmitters in the Rat Brain: Hae Kyu Kim, Seung Kyung Baeck, Sie Jeong Ryu, Inn Se Kim; Korean J Crit Care Med. 1998;13(1):33-42.

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Abstract PDF: Introduction: It was aimed to investigate the effect of chronic toluene exposure on amino acid neurotransmitters in the rat brain, corpus striatum.
METHODS
Twenty four male Sprague-Dawley rats were divided into one of three groups, control, acute, and chronic. Each groups was for the microdialysis to estimate the changes of amino acid neurotransmitters, aspartate, glutamate, and citrulline before, during, and after 3,000 ppm toluene exposure for 2 hours.
RESULTS
The results were as follows; 1) Aspartate and glutamate concentration were generally decreased in the toluene inhalation groups compared with the control group and more significantly decreased in chronic inhalation group than other groups. 2) Citrulline that expressed the activity of nitric oxide synthase and taurine as an inhibitory amino acid showed no significant differences between all groups. Based on these results, it is suggested that the decreasing excitatory amino acids, aspartate and glutamate, are partly contributed to the toxic mechanisms of toluene in rat brain.

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