Imidacloprid Poisoning

 

SUBSTANCE

imidacloprid poisoning 

 

Common name / Trade name

-       One kind of Neonicotinoid

 -益達胺; 霹靂掌; 金剛棒; 一帖靈; 勁厲害

-First-generation compounds appear to have significantly worse toxicity than second generation compounds despite both being classified as class II compounds (moderately hazardous) according to the WHO classification [1]

-Most were exposed by ingestion (93.3%) [2]

Involving SYSTEM

-Nervous system: nausea or vomiting with nervous system involvement [1] neurological effects (14.2%) [2]

- competitive inhibitor at the nicotinic acetylcholine receptors interfering with the transmission of impulses leading to fatigue and paralysis. [3]

-Renal: rhabdomyolysis resulting in acute kidney injury [4]

-GI: gastrointestinal symptoms (63.8%) with no corrosive injuries [2]

- other: ischemic and metabolic encephalopathy, multiorgan failure [4]

- arrhythmia: ventricular fibrillation [4]

-       neuropsychiatric sequelae [4]

 

Presentation

-       altered consciousness (32.1%) or muscle weakness (21.4%) [1]

-       drowsy but arousable, dyspnoeic, and profusely sweating [3]

-       Autonomic nervous system: stimulation causes sweating, dilated pupils, tachycardia, and hypertension [3]

-       nausea or vomiting, abdominal pain, drowsiness, headache, or dizziness, but some cases may be asymptomatic [4]

-        

Antidote / Treatment

-       GI decontamination. [3]

-       activated charcoal [4]

-       Intubation if unconscious [3]

-       No antidote, supportive care.

 

Disposition

-       predominantly male (60.7%) [1] no (18.4%) to mild (76.1%) toxicity [2]

-       A minority of patients required invasive care (28.6%) or invasive ventilation (25.0%) [1]

-       ICU care: in high lactate, RR> 24.7/min, GCS<11, SOFA score >3.4 [1]

-       cardiovascular effects (especially tachycardia and cardiac arrest), central nervous system effects (especially coma), dyspnea, and diaphoresis were significantly associated with mortality [2]

-       Mortality rate: 3.1% [2]

 

REFERENCES

1.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10949290/

2.https://pubmed.ncbi.nlm.nih.gov/33204096/

3.https://pubmed.ncbi.nlm.nih.gov/36987471/

4.    https://jmedicalcasereports.biomedcentral.com/articles/10.1186/s13256-022-03742-8

edited by Yu-Jang Su                  5 June 2024

 

Toluene Poisoning / Intoxication

 Substance

 Toluene

 

Common name or Trade name 

 C₆H₅CH₃

 C₇H₈

 甲苯: 汽車排放的廢氣， 油漆、油漆稀釋劑、指甲油、噴漆及黏著劑 possibly contains甲苯

 Route: inhalation of fumes, ingestion, or transdermal absorption [1, 2]

 Exposure: 77% were male and mean age was 23.5 years [3]

 

Involving system

 CNS: marked atrophy of the lower cervical spinal cord, thoracic spinal cord, and conus medullaris. [4]

     Reversible symmetrical white matter changes [ 5]

 Lung: aspiration pneumonitis. [2]

 CV system: potential arrhythmogenic effect of endogenous catecholamines, occasionally resulting in fatality.[6]

 Kidney: Renal glomerular injury (proteinuria)戊 renal tubular acidosis[2]

 Muscle: Rhabdomyolysis occurred in 80% of patients, probably due to hypokalemia and hypophosphatemia [3, 7]

 Cardiopulmonary failure [1]

 The cause of death was in all cases due to cardiac rhythm abnormalities. [7]

 

Presentation

   Chronic: mild cognitive impairment, hearing impairment, dysarthria, marked hyperreflexia of the limbs, spastic paraplegia, slight impairment of deep sensation, and urinary disturbance. 4 stimulus-sensitive spinal myoclonus [8]

   Acute: Severe hypokalemia and acidosis.

  . Biliary tract injury (alkaline phosphatase and gamma-glutamyl transpeptidase elevations) disproportional to hepatocellular injury is common.

Altered mental status, severe acidosis, hypokalemia and acute oliguric renal failure. [3, 7]

Symptomatic hypokalemia [2]

Adrenal insufficiency secondary to bilateral adrenal hemorrhage [9]

 

Antidote and Treatment

  No antidote

  Standardly supportive treatment

 

Disposition

    If asymptomatic, observe 6 hours, and discharge when the CXR is unremarkable.[2]

Poor in patients who have altered mental status, renal failure, severe acidemia and female gender, and patients with these characteristics should be considered to be treated in an intensive care unit. [7]

 

References

 

 [1]https://pubmed.ncbi.nlm.nih.gov/24164003/

[2]. Goldfrank’s toxicologic emergencies. 11^th ed. P. 1415~1417

[3].https://pubmed.ncbi.nlm.nih.gov/22642292/

 [4]https://pubmed.ncbi.nlm.nih.gov/32238742/

[5].https://pubmed.ncbi.nlm.nih.gov/25117062/

[6]. https://pubmed.ncbi.nlm.nih.gov/9140324/

[7].https://pubmed.ncbi.nlm.nih.gov/26282250/

   [8]https://pubmed.ncbi.nlm.nih.gov/10845207/

[9]https://pubmed.ncbi.nlm.nih.gov/9711204/

 

Edited by Yu-Jang Su   Nov 8, 2023

Amphetamine poisoning

 Substance

  Amphetamine

 

 

Common name

  安仔, 安公子 [1]

 

 

Involving system and Presentation

-          CV: flushing, diaphoresis, hypertension, vasoconstriction, lung edema, heart failure, shock. Tachycardia [1]

-          Neuro and psychiatric: agitation, delusion, hyperactivity, tremor, delirium, rigidity, acute psychosis [2], paranoid schizophrenia, hallucination. [1] Toxic encephalopathy. [3].

-          Hyperthermia, rhabdomyolysis, myoglobinuria. [1]

-          Acute kidney injury. [1]

-          acute porphyria. [4].

 

 

Antidote / Treatment

-          ACLS or shock, arrhythmia, hypertension, tachycardia.

-          Intubation when respiratory failure [1]

-          GI decontamination within 1 hour. Activated charcoal, 1gm/kg with laxative agent [1]

-          Benzodiazepine, barbiturate for seizure, delirium. [1]

-          Fever: sedative and external cooling. [1]

-          Rhabdomyolysis – hydration to keep urine output 1—2 ml./kg BW/hour. [1]

-          VPC – benzodiazepine +/- lidocaine. [1]

-          - hypotension – fluid challenge or inotropic agent. [1]

 

Disposition

-          PCO2 ≥ 51 mmHg, serum bicarbonate ≤ 22.6 mEq/L, and loss of consciousness on admission could be considered as prognostic factors of mortality [5]

-          The mortality rate was 5.4% [5]

 

 

References

 

[1]急性中毒救命術 三版 急診 急診醫學會p.119-128.

 

[2]. Bramness JG, Rognli EB. Psychosis induced by amphetamines. Curr Opin Psychiatry. 2016 Jul;29(4):236-41. doi: 10.1097/YCO.0000000000000254. PMID: 27175554.

 

[3]. Bojsen JA, Lunau L, Nguyen NT, Rasmussen BSB. [Amphetamine-induced toxic encephalopathy]. Ugeskr Laeger. 2022 May 23;184(21):V12210924. Danish. PMID: 35656615.

 

 

[4]. Kiew CK, Lam ASEL. Unexpected presentation of acute porphyria. BMJ Case Rep. 2021 Jun 29;14(6):e241580. doi: 10.1136/bcr-2021-241580. PMID: 34187794; PMCID: PMC8245470.

 

[5] Rahimi M, Lookzadeh S, Sadeghi R, Soltaninejad K, Shadnia S, Pajoumand A, Hassanian-Moghaddam H, Zamani N, Latifi-Pour M. Predictive Factors of Mortality in Acute Amphetamine Type Stimulants Poisoning; a Review of 226 Cases. Emerg (Tehran). 2018;6(1):e1. Epub 2018 Jan 10. PMID: 29503826; PMCID: PMC5827041.

 

Edited by Yu-Jang Su June 12, 2023

 

Glufosinate

 Substance

 

Glufosinate-Ammonium 13.5%SL

 

Common name / Trade name

 

強手(固殺草); 草銨膦

 

Involving system

-          Mechanism: glutamine synthetase-inhibiting [1]

-          Interferes with glutamate synthetase activity [2]

-          Neurotoxicity.

-          Mental disturbances [3]

-          Hematological changes

-          Gastrointestinal effects [3], nausea.

 

Presentation

-          Altered mental status [4] amnesia [2]

-          Fever [2]

-          Arrhythmia, [2]

-          Seizure, 31.5% [5]

-          higher initial ammonia levels. [6]

-          respiratory failure. [7]

-          Vasogenic edema in striatum [8]

-          Shock [2]

 

Antidote and Treatment

-          Activated charcoal, Carbomix [2].

-          IVF, monitoring urine output.

-          Intubation if respiratory failure

-          Monitoring.

-           supportive care.

-           benzodiazepine for seizure

-          Without antidote.

-          Hemodialysis [2]

 

Disposition

-          Observe 48 hours, [2]

-          Age > 70 years and GCS score < 9 at triage could be predictors of mortality in patients. [4]

-          An initial serum ammonia level >151 µg/dL was an independent early predictor of in-hospital mortality [9]

-          Older age (≥ 61 years; adjusted OR 4.9) and larger amount of glufosinate ingestion (≥ 13.9 grams; adjusted OR 25.2) were positively associated with the development of severe toxicity [10].

-          6.1% to 17.7% died following deliberate glufosinate ingestion. [2, 10]

 

References

 

[1]. https://pubmed.ncbi.nlm.nih.gov/36963955/

[2].Goldfrank’s Toxicology Emergencies p1478—79. 11^th ed.

[3] https://pubmed.ncbi.nlm.nih.gov/9491336/

[4] https://pubmed.ncbi.nlm.nih.gov/34392143/

[5]. https://pubmed.ncbi.nlm.nih.gov/28421825/

[6] https://pubmed.ncbi.nlm.nih.gov/36399183/

[7]. https://pubmed.ncbi.nlm.nih.gov/24044532/

[8] https://pubmed.ncbi.nlm.nih.gov/19581091/

[9]. https://pubmed.ncbi.nlm.nih.gov/31146590/

[10] https://pubmed.ncbi.nlm.nih.gov/22480254/

 

Edited by Yu-Jang Su May 1st, 2023. 

Theophylline Intoxication

 Substance

 -  theophylline intoxication.   

 -  (45.5%) had acute, (40.4%) had chronic, and (14.0%) had acute-on-therapeutic poisoning. [1]

Common name or Trade name

 -  definition: Therapeutic ranges are usually achieved between 10–20 μg/mL. Toxic effects are often seen above 20 μg/mL plasma concentrations. [2]

 

Involving system

-       Effect: diuretic, smooth muscle relaxant, cardiac, nervous system, and ventilator stimulant [2]

-       GI system: nausea, vomiting, gastrointestinal reflux [2]

-       Neuro: restlessness, and headache, convulsions (8.2%) [2, 3]

-       CV: severe cardiac arrhythmias (20.8%), hypotension (may result fromβ2-stimulated peripheral vasodilation) and even death occur at higher theophylline concentrations (usually 80–100 μg/mL). [1, 2]

 

Presentation 

-       severe cardiac arrhythmias, refractory hypotension, and convulsions [2]

-       Hypokalemia, hypercalcemia, hyperglycemia, and acidosis are metabolic disturbances that commonly occur after an acute overdose [2]

-       May complicate with Coma Blister. [4]

 

Antidote and Treatment

-       Gastrointestinal decontamination with activated charcoal. [2]

-       The use of beta-blockers is an acceptable approach to control tachydysrhythmias [2]

-       aggressive fluid administration + conventional vasopressors in cases of refractory hypotension.

-        

-       standard hemodialysis is a suitable alternative when severe theophylline toxicity [2].

Disposition 

-       Carefully DDx with a thyroid storm.  

-       4.2% fatality [D].  

REFERENCES

 [1]. Shannon M. Life-threatening events after theophylline overdose: a 10-year prospective analysis. Arch Intern Med. 1999 May 10;159(9):989-94. doi: 10.1001/archinte.159.9.989. PMID: 10326941.

 [2]. Aggelopoulou E, Tzortzis S, Tsiourantani F, Agrios I, Lazaridis K. Atrial Fibrillation and Shock: Unmasking Theophylline Toxicity. Med Princ Pract. 2018;27(4):387-391. doi: 10.1159/000490145. Epub 2018 Jun 22. PMID: 29936503; PMCID: PMC6170900.

[3]. Kopacz P, Kula K. Lethal poisoning with theophylline in the form of rectally administered tablets. Arch Med Sadowej Kryminol. 2014;64(3):158-64. doi: 10.5114/amsik.2014.48879. PMID: 25693173.

[4]. Tsokos M, Sperhake JP. Coma blisters in a case of fatal theophylline intoxication. Am J Forensic Med Pathol. 2002 Sep;23(3):292-4. doi: 10.1097/00000433-200209000-00019. PMID: 12198361.

 

edited by Yu-Jang Su            Dec 7, 2021