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Acute severe multiorgan dysfunction syndrome with oral acetamiprid poisoning
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MODEL
Journal of the Formosan Medical Association (2016) xx, 1e2
Available online at www.sciencedirect.com
ScienceDirect journal homepage: www.jfma-online.com
CORRESPONDENCE
Acute severe multiorgan dysfunction syndrome with oral acetamiprid poisoning Pengcheng Xing, Jianfei Xu, Lijuan Li, Ke Ma* Emergency Department, Shanghai Jiaotong University Affiliated Sixth Hospital, Shanghai, China Received 9 March 2016; received in revised form 17 June 2016; accepted 25 June 2016
Acetamiprid belongs to a new class of neonicotinoid insecticides that act as selective agonists at nicotinic acetylcholine receptors, causing insect paralysis and death.1,2 Despite its widespread use in China, the clinical symptoms and consequences of acute acetamiprid poisoning in humans have not been well described.3e5 Here, we report a case of a 48-year-old woman who consumed acetamiprid and developed severe multiorgan dysfunction. A healthy 48-year-old woman with no past disease history had a conflict with her family members and, with the intent of suicide, ingested approximately 30 mL of an insecticide formulation containing 5% acetamiprid. Immediately, the patient experienced dizziness, nausea, and mild abdominal distension, and vomited large amounts of gastric content several times. She was transported to our hospital by ambulance 30 minutes later. On arrival, she was fully conscious with stable vital signs. The patient’s initial electrocardiogram revealed sinus arrhythmia, with low ST segment depression at Leads I and V2eV5. Gastric lavage was performed immediately. However, 12 minutes after gastric lavage, she showed sudden limb tremor and involuntary head jerking to the left side. Her heartbeat decreased to 40e60 beats/min and blood pressure decreased to 70e90 mmHg/40e60 mmHg.
Conflicts of interest: The authors have no conflicts of interest relevant to this article. * Corresponding author. Emergency Department, Shanghai Jiaotong University Affiliated Sixth Hospital, No. 222 Three West Road Around Lake, New City Town, 201306 Pudong, Shanghai, China. E-mail address: [email protected] (K. Ma).
The patient’s electrocardiogram revealed atrial fibrillation with low ST segment depression at Leads III, avF, and V3eV6. Both pupils dilated to 5 mm in diameter, and their reactions to light slowed and subsequently disappeared. She had sobbing breaths with fine moist rales at the bottom of the lungs. Her blood leukocytes and neutrophils were much higher than the normal range, and blood gas analysis showed severe acidosis. The patient also experienced hepatic dysfunction and high blood amylase. We administered the following: atropine to prevent muscarinic symptoms due to a high acetylcholine level caused by acute organophosphate poisoning; 5% sodium bicarbonate to neutralize acidosis and decompose acetamiprid; glutathione and glycyrrhizin to protect liver and kidney function; and dopamine and norepinephrine to increase blood pressure. Ultimately, this patient was admitted to the emergency intensive care unit. During the next few days, she gradually regained consciousness and could consume a small amount of liquid food. She had a fever on Day 3, but she responded quickly to anti-infection treatment and recovered. During the process of recovery, the computed tomography scan and magnetic resonance imaging showed hypoxiceischemic damage at the bilateral frontal and basal ganglia (Figure 1). She had some difficulty in opening her eyes and narrow eye ptosis, possibly indicating oculomotor nerve damage. After group consultations with the other relevant departments in our hospital, she was administered oral methycobal once per day. One week after admission, all the relevant test results were normal and the patient was discharged from our hospital, with only narrow eye fission, but no difficulty with eye opening or movement; she displayed no tremor or convulsion.
http://dx.doi.org/10.1016/j.jfma.2016.06.008 0929-6646/Copyright ª 2016, Formosan Medical Association. Published by Elsevier Taiwan LLC. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). Please cite this article in press as: Xing P, et al., Acute severe multiorgan dysfunction syndrome with oral acetamiprid poisoning, Journal of the Formosan Medical Association (2016), http://dx.doi.org/10.1016/j.jfma.2016.06.008
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MODEL
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P. Xing et al. Although acetamiprid appears to have low toxicity in mammals, we should be aware of the dangers of human exposure.
References 1. Tomizawa M, Casida JE. Neonicotinoid insecticide toxicology: mechanisms of selective action. Annu Rev Pharmacol Toxicol 2005;45:247e68. 2. Takayama C. The history of insecticides and the transition of their production. Chudoku Kenkyu 2008;21:123e31 [In Japanese]. 3. Sun TQ, Zhao SG, Zhang XC. Two cases of acute acetamiprid poisoning. J Clin Emerg 2005;6:47e8. 4. Imamura T, Yanagawa Y, Nishikawa K, Matsumoto N, Sakamoto T. Two cases of acute poisoning with acetamiprid in humans. Clin Toxicol 2010;48:851e3. 5. Todani M, Kaneko T, Hayashida H, Kaneda K, Tsuruta R, Kasaoka S, et al. Acute poisoning with neonicotinoid insecticide acetamiprid. Chudoku Kenkyu 2008;21:387e90 [In Japanese].
Figure 1 Brain imaging in the current case of acute oral acetamiprid poisoning. (A, B) Computed tomography on Day 3 showed diffuse hypoxic ischemic injuries at the bilateral frontal and basal ganglia. (C, D) Magnetic resonance imaging on Day 7 showed diffuse hypoxiceischemic injuries at the bilateral basal ganglia (T2- and DWI hyperintensity). DWI Z diffusion weighted imaging.
Please cite this article in press as: Xing P, et al., Acute severe multiorgan dysfunction syndrome with oral acetamiprid poisoning, Journal of the Formosan Medical Association (2016), http://dx.doi.org/10.1016/j.jfma.2016.06.008
MODEL
Journal of the Formosan Medical Association (2016) xx, 1e2
Available online at www.sciencedirect.com
ScienceDirect journal homepage: www.jfma-online.com
CORRESPONDENCE
Acute severe multiorgan dysfunction syndrome with oral acetamiprid poisoning Pengcheng Xing, Jianfei Xu, Lijuan Li, Ke Ma* Emergency Department, Shanghai Jiaotong University Affiliated Sixth Hospital, Shanghai, China Received 9 March 2016; received in revised form 17 June 2016; accepted 25 June 2016
Acetamiprid belongs to a new class of neonicotinoid insecticides that act as selective agonists at nicotinic acetylcholine receptors, causing insect paralysis and death.1,2 Despite its widespread use in China, the clinical symptoms and consequences of acute acetamiprid poisoning in humans have not been well described.3e5 Here, we report a case of a 48-year-old woman who consumed acetamiprid and developed severe multiorgan dysfunction. A healthy 48-year-old woman with no past disease history had a conflict with her family members and, with the intent of suicide, ingested approximately 30 mL of an insecticide formulation containing 5% acetamiprid. Immediately, the patient experienced dizziness, nausea, and mild abdominal distension, and vomited large amounts of gastric content several times. She was transported to our hospital by ambulance 30 minutes later. On arrival, she was fully conscious with stable vital signs. The patient’s initial electrocardiogram revealed sinus arrhythmia, with low ST segment depression at Leads I and V2eV5. Gastric lavage was performed immediately. However, 12 minutes after gastric lavage, she showed sudden limb tremor and involuntary head jerking to the left side. Her heartbeat decreased to 40e60 beats/min and blood pressure decreased to 70e90 mmHg/40e60 mmHg.
Conflicts of interest: The authors have no conflicts of interest relevant to this article. * Corresponding author. Emergency Department, Shanghai Jiaotong University Affiliated Sixth Hospital, No. 222 Three West Road Around Lake, New City Town, 201306 Pudong, Shanghai, China. E-mail address: [email protected] (K. Ma).
The patient’s electrocardiogram revealed atrial fibrillation with low ST segment depression at Leads III, avF, and V3eV6. Both pupils dilated to 5 mm in diameter, and their reactions to light slowed and subsequently disappeared. She had sobbing breaths with fine moist rales at the bottom of the lungs. Her blood leukocytes and neutrophils were much higher than the normal range, and blood gas analysis showed severe acidosis. The patient also experienced hepatic dysfunction and high blood amylase. We administered the following: atropine to prevent muscarinic symptoms due to a high acetylcholine level caused by acute organophosphate poisoning; 5% sodium bicarbonate to neutralize acidosis and decompose acetamiprid; glutathione and glycyrrhizin to protect liver and kidney function; and dopamine and norepinephrine to increase blood pressure. Ultimately, this patient was admitted to the emergency intensive care unit. During the next few days, she gradually regained consciousness and could consume a small amount of liquid food. She had a fever on Day 3, but she responded quickly to anti-infection treatment and recovered. During the process of recovery, the computed tomography scan and magnetic resonance imaging showed hypoxiceischemic damage at the bilateral frontal and basal ganglia (Figure 1). She had some difficulty in opening her eyes and narrow eye ptosis, possibly indicating oculomotor nerve damage. After group consultations with the other relevant departments in our hospital, she was administered oral methycobal once per day. One week after admission, all the relevant test results were normal and the patient was discharged from our hospital, with only narrow eye fission, but no difficulty with eye opening or movement; she displayed no tremor or convulsion.
http://dx.doi.org/10.1016/j.jfma.2016.06.008 0929-6646/Copyright ª 2016, Formosan Medical Association. Published by Elsevier Taiwan LLC. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). Please cite this article in press as: Xing P, et al., Acute severe multiorgan dysfunction syndrome with oral acetamiprid poisoning, Journal of the Formosan Medical Association (2016), http://dx.doi.org/10.1016/j.jfma.2016.06.008
+
MODEL
2
P. Xing et al. Although acetamiprid appears to have low toxicity in mammals, we should be aware of the dangers of human exposure.
References 1. Tomizawa M, Casida JE. Neonicotinoid insecticide toxicology: mechanisms of selective action. Annu Rev Pharmacol Toxicol 2005;45:247e68. 2. Takayama C. The history of insecticides and the transition of their production. Chudoku Kenkyu 2008;21:123e31 [In Japanese]. 3. Sun TQ, Zhao SG, Zhang XC. Two cases of acute acetamiprid poisoning. J Clin Emerg 2005;6:47e8. 4. Imamura T, Yanagawa Y, Nishikawa K, Matsumoto N, Sakamoto T. Two cases of acute poisoning with acetamiprid in humans. Clin Toxicol 2010;48:851e3. 5. Todani M, Kaneko T, Hayashida H, Kaneda K, Tsuruta R, Kasaoka S, et al. Acute poisoning with neonicotinoid insecticide acetamiprid. Chudoku Kenkyu 2008;21:387e90 [In Japanese].
Figure 1 Brain imaging in the current case of acute oral acetamiprid poisoning. (A, B) Computed tomography on Day 3 showed diffuse hypoxic ischemic injuries at the bilateral frontal and basal ganglia. (C, D) Magnetic resonance imaging on Day 7 showed diffuse hypoxiceischemic injuries at the bilateral basal ganglia (T2- and DWI hyperintensity). DWI Z diffusion weighted imaging.
Please cite this article in press as: Xing P, et al., Acute severe multiorgan dysfunction syndrome with oral acetamiprid poisoning, Journal of the Formosan Medical Association (2016), http://dx.doi.org/10.1016/j.jfma.2016.06.008