ECG Changes on Poisoning / Intoxication

 ECG changes on poisoning/ intoxication

 

ECG	Substance	Date	Origin
Asystole	Lithium	1991	UK[1]
First degree AV block	Carbon monoxide Lithium	2013 2018	Riyadh[2] Taiwan[3] Kaohsiung Medical University Hospital
QRS complex widening	Hydrofluoric acid tricyclic antidepressant	2005 2016	USA [4] New Orleans[5] Spain [6]
QT interval prolongation	Hydrofluoric acid organophosphate	2005 2009	USA [4] Iran [7]
R wave in aVR ≥ 3 mm		2012	Spain [6]
Scooping of the T waves	Digoxin	2017	Lebanon[8]
Sinus bradycardia	Calcium channel blockade Beta-adrenergic receptor blockade
Sinus Dysfunction	Lithium	1995	Japan [9]
Tall T wave	Hydrofluoric acid	2001	Taiwan [10] MacKay Memorial Hospital.

 

References

1.      Ong AC, Handler CE. Sinus arrest and asystole due to severe lithium intoxication. Int J Cardiol. 1991 Mar;30(3):364-6. doi: 10.1016/0167-5273(91)90021-g. PMID: 2055679.

2.      Salih SB, Alenezi H, Alghamdi A. A case of first degree AV block in carbon monoxide poisoning patient. J Saudi Heart Assoc. 2013 Oct;25(4):255-9. doi: 10.1016/j.jsha.2013.05.004. PMID: 24198450; PMCID: PMC3818633.

3.      Chien SC, Liu KT, Wu YH. Lithium intoxication presenting as altered consciousness and arrhythmia with cardiogenic shock: A case report. Medicine (Baltimore). 2018 Nov;97(45):e13129. doi: 10.1097/MD.0000000000013129. PMID: 30407335; PMCID: PMC6250446.

 

4.      Holstege C, Baer A, Brady WJ. The electrocardiographic toxidrome: the ECG presentation of hydrofluoric acid ingestion. Am J Emerg Med. 2005 Mar;23(2):171-6. doi: 10.1016/j.ajem.2004.04.032. PMID: 15765339.

5.      Glancy DL. ECG Of the Month: Suicide. J La State Med Soc. 2016 Mar-Apr;168(2):66-7. Epub 2016 Apr 15. PMID: 27383860.

6.      Yates C, Manini AF. Utility of the electrocardiogram in drug overdose and poisoning: theoretical considerations and clinical implications. Curr Cardiol Rev. 2012 May;8(2):137-51. doi: 10.2174/157340312801784961. PMID: 22708912; PMCID: PMC3406273.

7.      Shadnia S, Okazi A, Akhlaghi N, Sasanian G, Abdollahi M. Prognostic value of long QT interval in acute and severe organophosphate poisoning. J Med Toxicol. 2009 Dec;5(4):196-9. doi: 10.1007/BF03178266. PMID: 19876851; PMCID: PMC3550412.

8.      Mansour MJ, Kalaoui M, Chammas E, Hamoui O, Fawaz T, AlJaroudi WA. Unusual digoxin toxicity with myocardial injury. J Electrocardiol. 2017 Nov-Dec;50(6):909-911. doi: 10.1016/j.jelectrocard.2017.07.013. Epub 2017 Jul 12. PMID: 28807352.

9.      Nakamura H, Takahashi F, Matsuzaka T, Tanaka H, Akashi N, Sato N, Kikuchi K. [A case of lithium induced sinus mode dysfunction]. Nihon Naika Gakkai Zasshi. 1995 Jan 10;84(1):127-9. Japanese. PMID: 7722356.

10.  Su YJ, Lu LH, Choi WM, Chang KS. Survival after a massive hydrofluoric acid ingestion with ECG changes. Am J Emerg Med. 2001 Sep;19(5):458-60. doi: 10.1053/ajem.2001.24503.

edited by Yu-Jang Su            

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.

SSRI (selective serotonin reuptake inhibitor)

 SSRI (selective serotonin reuptake inhibitor) 血清素再吸收阻斷劑

SUBSTANCE

 

-          Newer and safer antidepressant compared to TCA [1].

-          Lower ADR than TCA.

 

 

Common name or Trade name 

 

-          Fluvoxamine、Paroxetine、Sertraline、Citalopram、Escitalopram、Fluoxetine。

 

 

Involving SYSTEM

 

-          Serotonin,  about 98% in extra-CNS [2]。

-          A long elimination half-life, with sustained biological activity due to active metabolites

-          In overdose, SSRI elimination times are further prolonged by the saturation of metabolic enzymes and by delayed absorption, especially for sustained-release preparations.

-          Electrolyte imbalance: hyponatremia, easily seen in the elderly [3].

-          Neural system: extra-pyramidal, hyperreflexia, Clonus, myoclonus [4].

-          Respiratory system: failure. Cough.

-          Gastrointestinal system: nausea, upset.

 

Presentation

 

-          Cause vomiting, mild CNS depression, or tremor.

-          Hyponatremia.

-          Unstable blood pressure. Arrhythmia. VT. Arrest, QRS QTc prolongation, Torsades de pointes [5].

-Bradycardia, hypotension: Fluvoxamine (Luvox)

- hyperreflexia, Clonus, myoclonus.

- Sweating, agitation.

- fever, coma, seizure (1.9%) [6].

 

Antidote and Treatment 

 

-          BLS, gastric lavage < 1 hr.  

-          Activated charcoal.

-          Not recommended for laxative.

-ACLS, inotropic agent.

-Nitroglycerin或Nitroprusside for hypertension。

-  magnesium sulfate 2 g IV over 2 min for Torsades de points

-  wide QRS: NaHCO3 1 to 2 mEq/kg IV push

- (benzodiazepine, BZD) for seizure.

- Serotonin antagonist:

     -Cyproheptadine (oral form; sedation) [7].

- (Extrapyramidal signs): Diphenylhydramine 50mg bid。

 

Disposition

 

-          Suspicious: observe 6-8 hours with ECG monitoring, if no symptoms, then may be discharged.

-          Citalopram, need observe longer to 12hours, observe arrhythmia / convulsion [8].

 

REFERENCES

 

[1]. https://pubmed.ncbi.nlm.nih.gov/35206480/

[2]. https://pubmed.ncbi.nlm.nih.gov/19361459/

[3]. https://pubmed.ncbi.nlm.nih.gov/34483534/

[4]. https://pubmed.ncbi.nlm.nih.gov/23391344/

[5]. https://pubmed.ncbi.nlm.nih.gov/31845095/

[6]. https://pubmed.ncbi.nlm.nih.gov/30521236/

[7]. https://pubmed.ncbi.nlm.nih.gov/20833944/

[8]. https://pubmed.ncbi.nlm.nih.gov/33489987/

 

Edited by Yu-Jang Su                 May 26, 2022

海檬果

Substance

Cerbera Odollam

Photo: https://www.123rf.com/photo_73477720_seed-of-pong-pong-tree-suicide-tree-pong-pong-othalanga-cerbera-odollam-.html

 

Common name or Trade name

Pong-Pong Seeds

海檬果.

Cerberus Tree

Sea Mango

Othalanga [1]

Suicide tree

 

Involving system

Cardiac glycosides related arrhythmia

Strong cardiotoxic effects [1] 


Presentation

Nausea, vomiting, thrombocytopenia [1]

Hyperkalemia [1, 2]

Heart block [2] ECG abnormalities [1].

Death [2]

 

Antidote and Treatment

 

Supportive therapy [1]

Atropine followed by temporary pacemaker insertion [1]

Administration of digoxin immune Fab may be considered in severe cases [1]  
Disposition

Hospitalization.

  References

[1] Menezes RG, Usman MS, Hussain SA, et al. Cerbera odollam toxicity: A review. J Forensic Leg Med. 2018;58:113–116. doi:10.1016/j.jflm.2018.05.007 

[2] Wermuth ME, Vohra R, Bowman N, Furbee RB, Rusyniak DE. Cardiac Toxicity from Intentional Ingestion of Pong-Pong Seeds (Cerbera Odollam). J Emerg Med. 2018;55(4):507–511. doi:10.1016/j.jemermed.2018.05.021


-- edited 21th Feb, 2020 Yu-Jang Su.

 

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

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