研討會訊息: 強化醫療端新興濫用藥物監測機制計畫」 藥物濫用個案醫療救護訓練

Aug 11, 2020 高雄場: 

https://www.sem.org.tw/Activity/Details/24070

Aug 18, 2020 台中場: 

https://www.sem.org.tw/Activity/Details/24069

主辦單位: 社團法人台灣急診醫學會 

指導單位: 衛生福利部 食品藥物管理署

July 20, 2020 台北場:

Nitrous Oxide Poisoning

Substance

Nitrous oxide

Common name or Trade name

一氧化二氮

笑氣

Involving system

-          Non-specific: dizzy. Headache. [1]

-          Consciousness: confusion, mental altered, coma. 

-          Liver: hepatitis [2]

-          Vit B 12 deficiency [1, 3 ,4, 5]

-          Nerve: myelopathy [2]

Presentation

-          Asphyxia when acute poisoning

-          Hypoxemia [6]

-          Myocardial infarcts, asystole.

-          Chest tightness. Cough, palpitation. [1]

-          ECG: myocardial ischemia.

-          MYELOPATHY [3, 5]

-          megaloblastic anemia, leukopenia, thrombocytopenia [1]

-          Death [1, 6]

-          Allergy: fever, chills, hives, wheezing, difficulty breathing

-          tingling or numbness in your fingers, toes, and limbs resulting from lacking Vit. B12 and anemia. [1]

-          high methylmalonyl CoA and homocysteine [4]

-          acute psychosis [4].

-          Slow NCV [1]

Antidote and Treatment

-          cause permanent neurological damage if not treated promptly

-          oxygen

-          intubate when respiratory failure. [1]

-          ACLS, CPCR if necessary / indicated. [1]

-          Avoid BZD/ sedative agent [1]

-          IVD or IM VitB12 1000μg/d* 5 days then per week 1000μg Vit B12 IM * 4-8 weeks [7].

Disposition  

-          Consult Neurology/ Toxicology /Poison Center.

- Follow-up at Neurology OPD and ever reported supplement time of Vit B12: two months.

References

[1]. 急性中毒救命術. 急診醫學會.三版.p.157—161.

[2]. Gullestrup A, Jensen RB, Bøgevig S, Nilsson PM. Ugeskr Laeger. 2019;181(20):V12180890.

[3]. Lin RJ, Chen HF, Chang YC, Su JJ. Subacute combined degeneration caused by nitrous oxide intoxication: case reports. Acta Neurol Taiwan. 2011;20(2):129-137.

[4]. Sethi NK, Mullin P, Torgovnick J, Capasso G. Nitrous oxide "whippit" abuse presenting with cobalamin responsive psychosis. J Med Toxicol. 2006;2(2):71-74. doi:10.1007/BF03161175

[5]. Lan SY, Kuo CY, Chou CC, et al. Recreational nitrous oxide abuse related subacute combined degeneration of the spinal cord in adolescents - A case series and literature review. Brain Dev. 2019;41(5):428-435. doi:10.1016/j.braindev.2018.12.003

[6]. Bäckström B, Johansson B, Eriksson A. Death from Nitrous Oxide. J Forensic Sci. 2015;60(6):1662-1665. doi:10.1111/1556-4029.12879

[7]. Pugliese RS, Slagle EJ, Oettinger GR, Neuburger KJ, Ambrose TM. Subacute combined degeneration of the spinal cord in a patient abusing nitrous oxide and self-medicating with cyanocobalamin. Am J Health Syst Pharm. 2015;72(11):952-957. doi:10.2146/ajhp140583

~~ June 18, 2020 Yu-Jang Su

Toluene poisoning

Substance

Toluene

Common name or Trade name

- 甲苯 C7H8

- 從原油中提煉出來

- 用於油漆類, 黏著劑, 指甲油, 塗料, 清潔劑裡 [1]

 Involving system

- heart : life-threatening dysrhythmias, such as ventricular tachycardia and ventricular fibrillation. Bradycardia [2] , longer QT in chronic poisoning [3]

- hematopoietic: aplastic anemia, acute myelogenous leukemia, and multiple myeloma. [4]

- liver: hepatitis [5].

- kidney: metabolic acidosis. [6]

- neurology : headache, and causes euphoria followed by depression

- pulmonary system: destroying alveolar and capillary membranes. This results in vascular permeability and edema.

- muscle: causes hypokalemia leading to muscle weakness and if low enough, muscle paralysis. Rhabdomyolysis is a common complication (80%). [3]

Presentation 

 - 頭痛、恍惚與喪失記憶, ataxia, lethargy and coma. Dizziness, confusion, [1]

 - SOB, Wheezing . 

 - Ventricular arrhythmias. [2] 

 - Nausea, abdominal pain, vomiting.

 - Muscle weakness and paralysis, and rhabdomyolysis 

Antidote and Treatment

- no specific antidote 

- No benefit to gastric lavage or activated charcoal 

- 20%直接由肺的呼吸而排出，有些甲苯會代謝成更具水溶性、且毒性較低的馬尿酸 (hippuric acid) 經由尿液排出 

- Secure airway. 

- oxygen if SOB, wheezing. 

- Broncho-dilator. Beta-2 agonist. 

- MV support if respiratory failure. 

- IVF for hypotension / observation. 

- treat arrhythmia according to ACLS

 Disposition 

- depends on intoxicated dose.

- ICU when altered mental state, renal failure, severe acidemia [3]

- female gender could be associated with a poor outcome [3]

References

[1]. Filley CM. Toluene abuse and white matter: a model of toxic leukoencephalopathy. Psychiatr Clin North Am. 2013;36(2):293‐302. doi:10.1016/j.psc.2013.02.008

[2]Einav S, Amitai Y, Reichman J, Geber D. Bradycardia in toluene poisoning. J Toxicol Clin Toxicol. 1997;35(3):295‐298. doi:10.3109/15563659709001214

[3]. Peckham T, Kopstein M, Klein J, Dahlgren J. Benzene-contaminated toluene and acute myeloid leukemia: a case series and review of literature. Toxicol Ind Health. 2014;30(1):73‐81. doi:10.1177/0748233712451764

[4]. Park CK, Kwon KT, Lee DS, et al. Taehan Kan Hakhoe Chi. 2003;9(4):332‐336.

[5]. Kamijima M, Nakazawa Y, Yamakawa M, et al. Metabolic acidosis and renal tubular injury due to pure toluene inhalation. Arch Environ Health. 1994;49(5):410‐413. doi:10.1080/00039896.1994.9954994

[6]. Camara-Lemarroy CR, Rodríguez-Gutiérrez R, Monreal-Robles R, González-González JG. Acute toluene intoxication--clinical presentation, management and prognosis: a prospective observational study. BMC Emerg Med. 2015;15:19. Published 2015 Aug 18. doi:10.1186/s12873-015-0039-0

~~ May 22, 2020 Yu-Jang Su

Carbon Monoxide Poisoning

Substance

carbon monoxide

Common name or Trade name  

一氧化碳

      Involving system

CO produces toxicity by binding to hemoglobin, thereby reducing oxygen-carrying capacity, and by binding to myoglobin, which may impair cardiac output and result in cerebral ischemia [1].

Presentation

   Asymptomatic                                                                HbCO 0—10% 

   Mild headache, respiratory distress HbCO 10—20%

    Headache, nausea. Lethargy, weakness HbCO 20—30%

   Nausea, vomiting, syncope, weakness HbCO 30—40%

   Unconsciousness seizure, arrhythmia. HbCO 50%

   Deep coma                                                                                   HbCO 60%

   Fatal 70% [2] 

   Fetus HbCO level higher than maternal HbCO 15%[2]

Antidote and Treatment

   ACLS if hemodynamic unstable.

    NRM or mask 100%

HBO (hyperbaric oxygenation) when coma. AMS. ABG pH<7.1, Cardiac ischemia. HbCO> 25%; pregnant female HbCO> 20% [2]

   Disposition 

        Admission if complication with rhabdomyolysis, aspiration pneumonia, AMS, etc.

References

[1]. Olson KR. Carbon monoxide poisoning: mechanisms, presentation, and controversies in management. J Emerg Med. 1984;1(3):233–243. doi:10.1016/0736-4679(84)90078-7

[2].急性中毒救命術, 第三版. P.309—17.

~~ April, 26th, 2020.  Yu-Jang Su