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

Chloroquine poisoning

Substance

Chloroquine

Common name or Trade name, used in

-          Chloroquine is a derivative of 4-aminoquinoline [1]

-          toxic dose > 20mg/kg [2]

-          fatal when > 5 gm [3]

-          Used in the malaria prophylaxis [1]

-          treatment of malaria, some connective tissue diseases, COVID-19 infection [1, 4]

 

Involving system

-          cardiovascular system [2].

-          altered mental status [2]

-          apnea, hyperventilation [2]

-          quinidine-like action [2].

-          negative inotropic action [2]

 

Presentation

-          Seizure [1]

-          Ventricular fibrillation [1]

-          QRS widening [5]

-          QTc prolongation [1]

-          Shock [5]

-          Cardiovascular collapse. [5] OHCA (15%) [6]

Antidote and Treatment

-          IVF + adrenalin, ACLS [5, 7]

-          NaHCO3 –

-          mechanical ventilation if respiratory failure [5, 7].

-          intravenous administration of diazepam and epinephrine [5]

-          diazepam dose (1 mg/kg) [7, 8] stat and 5—10mg/hrs. * 48 hours. Mechanism: increased chloroquine concentration in the blood, but decreased it in the heart muscle [2].

-          ECMO [5]

Disposition

-          MICU if hemodynamic change/ AMS [5]

-          overall mortality for all degrees of intoxication: 8.4% to 10% [6, 7]. 

References

 

[1] Ciszowski K, Winnik L, Groszek B, Kłys M, Kołodziej J. Ostre zatrucie chlorochina--rzadkie, ale zawsze powazne: opis przypadków i przeglad literatury [Acute chloroquine intoxication--rare, but always serious: case reports and literature review]. Przegl Lek. 2005;62(6):501–507.

[2]. Rajah A. The use of diazepam in chloroquine poisoning. Anaesthesia. 1990;45(11):955–957. doi:10.1111/j.1365-2044.1990.tb14629.x

[3] Riou B, Barriot P, Rimailho A, Baud FJ. Treatment of severe chloroquine poisoning. N Engl J Med. 1988;318(1):1–6. doi:10.1056/NEJM198801073180101

[4] Hu TY, Frieman M, Wolfram J. Insights from nanomedicine into chloroquine efficacy against COVID-19 [published online ahead of print, 2020 Mar 23]. Nat Nanotechnol. 2020;10.1038/s41565-020-0674-9. doi:10.1038/s41565-020-0674-9

[5] Bagate F, Radu C, Mekontso Dessap A, de Prost N. Early extracorporeal membrane oxygenation for cardiovascular failure in a patient with massive chloroquine poisoning. Am J Emerg Med. 2017;35(2):. doi: 10.1016/j.ajem.2016.08.058

[6] Clemessy JL, Taboulet P, Hoffman JR, et al. Treatment of acute chloroquine poisoning: a 5-year experience. Crit Care Med. 1996;24(7):1189–1195. doi:10.1097/00003246-199607000-00021

[7] Clemessy JL, Lapostolle F, Borron SW, Baud FJ. Intoxication aiguë à la chloroquine [Acute chloroquine poisoning]. Presse Med. 1996;25(31):1435–1439.

[8]. Altrock G, Lange A, Münster P. Akute Chloroquin-Intoxikation [Acute chloroquine poisoning]. Dtsch Med Wochenschr. 1997;122(8):225–228. doi:10.1055/s-2008-1047601

 

-- 26th March, 2020  Yu-Jang Su

 

 

Organophosphate poisoning

Substance

Organophosphate

Commonly used as insecticides

Common name or Trade name

磷酸酯或有機磷

Involving system

-Mechanism: They bind to acetylcholinesterase (AChE), also known as red blood cell (RBC) acetylcholinesterase, and render this enzyme non-functional [1]

-Aging: After some period of time, the acetylcholinesterase-organophosphorus compound undergoes a conformational change, known as "aging," which renders the enzyme irreversibly resistant to reactivation by an antidotal oxime [2]
- possible poisoning: decreased > 50% plasma cholinesterase or RBC cholinesterase 
- severe poisoning:  decreased > 90% plasma cholinesterase or RBC cholinesterase 

Presentation

SLUDGE/BBB – Salivation, Lacrimation, Urination, Defecation, Gastric Emesis, 

                            Bronchorrhea, Bronchospasm, Bradycardia

DUMBELS – Defecation, Urination, Miosis, Bronchorrhea/Bronchospasm/Bradycardia, 

                      Emesis, Lacrimation, Salivation [3] 

 
Antidote and Treatment

- GI decontamination: poisoning less than 1 hour

- activated charcoal 1gm/Kg BW.

- Atropine: 1 to 3 mg IV for adults and 0.05 mg/kg IV for children

If no effect is noted, the dose should be doubled every three to five minutes until pulmonary muscarinic signs and symptoms are alleviated [4]

- Pralidoxime: 30 mg/kg in adults, and 25 to 50 mg/kg for children, Pralidoxime should NOT be administered without concurrent atropine in order to prevent worsening symptoms due to transient oxime-induced acetylcholinesterase inhibition [5]

Disposition

Endotracheal intubation if the respiratory failure or markedly depressed mental status

Admission to the intensive care unit if hemodynamic  changes / AMS / respiratory failure.

References

[1] Khurana D, Prabhakar S. Organophosphorus intoxication. Arch Neurol 2000; 57:600.

[2] Eddleston M, Szinicz L, Eyer P, Buckley N. Oximes in acute organophosphorus pesticide poisoning: a systematic review of clinical trials. QJM 2002; 95:275.

[3] Sidell FR. Clinical effects of organophosphorus cholinesterase inhibitors. J Appl Toxicol 1994; 14:111.

[4] Konickx LA, Bingham K, Eddleston M. Is oxygen required before atropine administration in organophosphorus or carbamate pesticide poisoning? - A cohort study. Clin Toxicol (Phila) 2014; 52:531.

[5] Johnson MK, Jacobsen D, Meredith TJ, et al. Evaluation of antidotes for poisoning by organophosphorus pesticides. Emerg Med 2000; 12:22.

--20^th, March 2020 Sheng-Teck Tan, Yu-Jang Su