Paraquat poisoning

 

Substance

-  Paraquat.

Common name or Trade name

-   巴拉刈. 速草淨, 全草滅, 草蕪松 [1]

Involving system

-      Gastrointestinal – oral, transient liver toxicity, jaundice. [1]

- lung: pulmonary fibrosis [1]

- kidney: ATN, AKI [1]

- heart: hypotension, myocarditis, arrhythmia. [1]

- AMS- mental change. Seizure. Coma. [1]

Presentation 

-       Nausea, vomiting. [1]

-       Diarrhea [1]

-       Dyspnea [1]

-       Pneumoperitoneum, pneumomediastinum [2].

-       Seizure [1]

-       jaundice [1]

-       Coma [1]

-       Asystole. [1]

Antidote and Treatment

-       Decontamination: remove clothes, washing [1].

-       NG irrigation within 1 hour [1].

-       Fuller earth, 100—150 gm. Child: 2 gm/kg BW. Activated charcoal 25—100gm, child 25—50 gm [1].

-       Hemoperfusion within 2—4 hours [1].

-       Hemodialysis if renal failure [1].

-       No antidote.

Disposition 

-       MICU in confirmed poisoning cases with hemodynamic unstable.

-       25% to 44% of mortality rate in pregnant women [3].

REFERENCES

1.      急診醫學會AILS三版P.85—94.

 

2.      James N, Bakshi R, Rudresh SS, Kaushik K, Ghumaan KS, Pannu AK. Pneumoperitoneum from pneumomediastinum in paraquat poisoning. Trop Doct. 2020 Sep 30:49475520960872. doi: 10.1177/0049475520960872. Epub ahead of print. PMID: 32998627.

 

3.      Trakulsrichai S, Paisanrodjanarat B, Sriapha C, Tongpoo A, Udomsubpayakul U, Wananukul W. Clinical outcome of paraquat poisoning during pregnancy. Clin Toxicol (Phila). 2019 Aug;57(8):712-717. doi: 10.1080/15563650.2018.1549328. Epub 2019 Jan 28. PMID: 30689470.

edited by Yu-Jang Su  Feb 27, 2021. 

毛地黃中毒

 

Substance

-  Digitalis.  

- 強心配糖體之動植物:夾竹桃, 鈴蘭, 紅海蔥, 海檬果, 玉竹, 馬利筋, 萬年青, 側金盞花, 黑眶蟾蜍, 中華大蟾蜍  [1] 

Common name or Trade name

-  digoxin. 

Involving system

-       Inhibit Na, K ATPase, increased intracellular Ca. (By increasing in intracellular sodium concentration competes for calcium through this exchange mechanism leading to an increase in intracellular calcium concentration.)  

-       Increment heart contractility.

Presentation 

- mean age of patient: 76.1 ± 12.2 years old, comorbidities with CHF: 66.4%; atrial fibrillation: 54%. [2]

-  hyperkalemia. [1]

- GI: GI upset, nausea. Diarrhea, weakness, dehydration [1]. Abdomen pain. [2]

- Neuro: altered mental status, headache, lethargy, confusion, syncope, hallucination, coma, convulsion.

- CV: arrhythmia, AV block. Bradycardia. [1] ECG: scooping ST-T complex. [3]

- eye: colored floaters, major in yellow [4].

Antidote and Treatment

-       NG irrigation within 1 hr

-       Activated charcoal. (Carbomix 12.5 gm/ hr) [1]

-       Hemodynamic change, arrhythmia, and cardiac arrest: digoxin Fab-specific Abs.

-IVF + dopamine infusion for hypotension. [1]

-       50% Glucose + HRI for hyperkalemia. (3 amps 50%Glucose + HRI 8U)

-       No definite effect by hemoperfusion and hemodialysis.

Disposition 

-   ICU if hemodynamic unstable.

 

REFERENCES

[1]. 急性中毒救命術, 台灣急診醫學會. P.175—182.

[2]. Limon G, Ersoy G, Oray NC, Bayram B, Limon O. Retrospective evaluation of patients with elevated digoxin levels at an emergency department. Turk J Emerg Med. 2016 Mar 14;16(1):17-21. doi: 10.1016/j.tjem.2015.10.001. PMID: 27239633; PMCID: PMC4882205.

[3]. Castello LM, Negro S, Santi F, Zanotti I, Vidali M, Bagnati M, Bellomo G, Avanzi GC. Accidental digitoxin intoxication: an interplay between laboratory and clinical medicine. Biochem Med (Zagreb). 2012;22(3):380-4. doi: 10.11613/bm.2012.040. PMID: 23092069; PMCID: PMC3900044.

[4]. Shi L, Sun LD, Odel JG. Colored floaters as a manifestation of digoxin toxicity. Am J Ophthalmol Case Rep. 2018 Mar 2;10:233-235. doi: 10.1016/j.ajoc.2018.02.024. PMID: 29780940; PMCID: PMC5956671.

edited by Yu-Jang Su            Jan 29, 2021

 

HF poisoning

 

Substance

-      Hydrofluoric acid

Common name or Trade name

-       氫氟酸

- 用途: 磨光玻璃,  金屬除鏽，半導體工業[1].

 

Involving system

- depends on the route of exposure  

 - electrolyte imbalance

-       Skin necrosis if contact injury.

 

Presentation 

-     hypocalcemia [1,2]

- hyperkalemia [1]

- hypomagnesemia [1]

- arrhythmia, VT, Vf [2].

-extreme high T wave in ECG [2]

 

Antidote and Treatment

- skin decontamination [1]; activated charcoal is not indicated.

-     Sincal; Calcium gluconate [2]

- milk in ingested HF case [2].

- NG decompression rather than irrigation [1].

- ACLS

Disposition 

-       lethal dose: 1.5gm, or 20mg/kg.

  - ICU care when arrhythmia/life-threatening condition or massive burn injury,

50% solution > TBSA 1%;

TBSA > 5%;

> 60% solution inhalation injury.

Swallowing/ingestion injury.

 

REFERENCES

[1]. 急診醫學會, AILS三版, p. 247—254.

[2]. Su YJ, Lu LH, Choi WM, Chang KS. Survival after massive hydrofluoric acid ingestion with ECG changes. Am J Emerg Med. 2001 Sep;19(5):458-60. doi: 10.1053/ajem.2001.24503. Erratum in: Am J Emerg Med. 2009 Jan;27(1):126. PMID: 11555812.

 

Dec 28, 2020, edited by Yu-Jang Su.

Methanol Poisoning

 

Substance

-       Methanol

-       CH₃OH

 

Common name or Trade name

-       甲醇

-       Used in 抗凍劑, 溶劑, 皮革工廠, 染料塗料

 

Involving system [1]

-       Metabolic acidosis. lethargy

-       GI system:

-       Neurologic system: after poisoning 8 months to 2 years, secondary Parkinsonism.

-       Eye: Retinopathy, blindness.

 

 Presentation [1]

-       6—12 hours, 18—24 hours even 60 hours. After ingestion.

-       Blurred vision.

-       Stupor, coma.

-       Headache

-       SOB

-       Nausea. Abdomen pain, diarrhea.

-       High anion gap acidosis.

-       High osmolar gap acidosis

 

Antidote and Treatment [2]

-       Decontamination.

-       Carbomix (activated charcoal) is useless.

-       Intubation while acute respiratory failure.

-       ACLS

-       Ethanol: competition of aldehyde dehydrogenase, 1 gm/kg BW= 紹興(18%) 6ml/ kg BW till seral ethanol level 100—150 mg/dl. [1]

-       Fomepizole: 10—20 mg/kg / day * 3—5 days. (inhibit metabolism of methanol). [1]

-       Hemodialysis. [1]

-       Folic acid: 50 mg IV every 4 - 6 hours until toxicity resolves (increase formic acid oxidation into carbon dioxide and water). [3]. https://www.ebmconsult.com/articles/methanol-toxicology

-       Leucovorin dose: 1 mg/kg (50-70 mg adults) IV q4-6hr. (Folinic acid or leucovorin, the biologically active forms of folic acid, must be used for reversing toxicity due to dihydrofolate reductase inhibitors.)

Disposition 

-       Admit to ICU if severe acidosis, SOB, respiratory failure, or acute kidney injury  

-       Consult ophthalmologist if there is symptoms of eye.

  

REFERENCES

[1]. 急診醫學會, AILS 三版 p.255—265

[2]. Barceloux DG, Bond GR, Krenzelok EP, Cooper H, Vale JA; American Academy of Clinical Toxicology Ad Hoc Committee on the Treatment Guidelines for Methanol Poisoning. American Academy of Clinical Toxicology practice guidelines on the treatment of methanol poisoning. J Toxicol Clin Toxicol. 2002;40(4):415-46. doi: 10.1081/clt-120006745. PMID: 12216995.

[3]. Lim CS, Bryant SM. Forgoing the Folate?-Contemporary Recommendations for Methanol Poisoning and Evidence Review. Am J Ther. 2016 May-Jun;23(3):e850-4. doi: 10.1097/MJT.0000000000000059. PMID: 24531405.

edited  by Yu-Jang Su          Nov 28, 2020