Xylene poisoning

 

Substance:

• Name: Xylene (二甲苯)
• Common Uses: Solvent in chemical industries and de-waxing agent in pathology labs.

Common Name:

• Common Name: Xylene

Involving System:

• Primary Systems Affected: Central Nervous System (CNS), Respiratory System, Skin, Liver, Kidneys

Presentation:

1. Acute Exposure:

   • Low Concentration (50 ppm or less): Mild symptoms like headache, dizziness, and nausea.
   • Moderate Concentration (50–200 ppm): CNS symptoms, reduced concentration, drowsiness, respiratory irritation (sore throat, cough).
   • High Concentration (>200 ppm): Severe CNS depression, dizziness, ataxia, fainting, liver and kidney stress.
   • Skin Exposure: Dry skin, dermatitis, possible burns from high concentrations.
   • Ingestion: CNS suppression, gastrointestinal irritation, coma, and respiratory depression.

2. Chronic Exposure:

   • Nervous System: Memory loss, difficulty concentrating, mood changes.
   • Liver & Kidneys: Metabolic burden leading to damage.
   • Reproductive Toxicity: Decreased sperm count, menstrual irregularities in women.

Antidote:

• No specific antidote.
• Treatment involves supportive care, including oxygen therapy for inhalation exposure, decontamination of skin, and monitoring of liver and kidney function.

Disposition:

• Treatment and Monitoring: Symptomatic management including IV fluids, monitoring for CNS, respiratory, liver, and kidney damage. Active charcoal 1 gm/kg may be administered if ingested.

References:

• For additional case studies and fatal incidents: PubMed link.

Edited by Yu-Jang Su    2 Oct, 2024.

異氰酸酯 (Isocyanate) poisoning / intoxication

 

SUBSTANCE

異氰酸酯 (Isocyanate)

Component of organic chemistry, making them perceived as compounds with high potential for use in both the laboratory and industry. Such as 膠黏劑、PU樹脂、塗料、密封劑。 以MDI、TDI和多元醇預聚的產品系列。

Application: 汽車座椅方向盤等周邊、運動器材、 家俱、寢具、塗料、凝膠、滾輪、刮刀、密封件、防水材、PU跑道、再生海綿膠、人造草坪膠、軟包裝腹膜膠等用途 [1]。

 

Common name / Trade name

異氰酸酯

Exposure to methyl isocyanate: via route of inhalation or dermal absorption. [2]

 

Involving SYSTEM

 

Animal report: Imbalance of both the brain and plasma amino acids, suggesting neurotoxic and systemic effects [3].

Rat study report: Oncogenicity - Pulmonary adenomas were found in 6 males and 2 females, and pulmonary adenocarcinoma in one male in the high dose group. [4]

 

Presentation

 

Toxicity might develop over 1 to 4 hours after exposure. [2]

Toxic effect, consequently causing an inflammatory infiltrate in the

bronchial wall (Lemiere et al., 1996),

goblet cell hyperplasia, subepithelial fibrosis (Pons et al., 1999),

mucus plugs (Bucher et al., 1987),

and, consequently, allergic asthma. [1]

cough, dyspnea, chest pain, lacrimation, eyelid edema, and unconsciousness. [2]

 

Antidote / Treatment

 

There is no antidote for methyl isocyanate.

 

Treatment consists of removal of the victim from the contaminated area and support of respiratory and cardiovascular functions.

 

 

Disposition

 

At least observation 6 hours, in some severe case, signs and symptoms of methyl isocyanate might progress over the next 24 to 72 hours to include acute lung injury, cardiac arrest, and death [2].

 

REFERENCES

 

1. https://pubmed.ncbi.nlm.nih.gov/38761928/ and  https://www.sciencedirect.com/science/article/abs/pii/S0048969724033977?via%3Dihub

 

2 CDC emergency preparedness and response.

 

3: https://pubmed.ncbi.nlm.nih.gov/8956091/

 

4. Toxicology: Isocyanates Profile. U.S. Environmental Protection Agency.

 

Edited by Yu-Jang Su    2 Sep, 2024.

 

Acute Kidney Injury prevention related to poisoning and intoxication

Some reminding and precautions 

in using medication and avoiding substances related to acute kidney injury:

Glafenin

Vancomycin

Aminoglycosides

Gentamicin

Lithium

Contrast-induced

Snakebite

Hymenoptera stings

Herbicides

Ethylene glycol intoxication

New psychoactive substances (NPSs)

Cocaine-induced AKI

Heroin

Amphetamine, methamphetamine, and 3,4 methylenedioxymethamphetamine (MDMA, ecstasy)

 

Reference: https://www.mdpi.com/1648-9144/60/8/1302

PubMed: https://pubmed.ncbi.nlm.nih.gov/39202583/

Edited by Yu-Jang Su  15 Aug 2024 

Heloderma suspectum envenomation

 

Bitten injury by Heloderma suspectum

希拉毒蜥 咬傷

 

SUBSTANCE

-The venom contains some protein and nonprotein components including serotonin, a bradykinin-releasing substance, protease, hyaluronidase, helodermin, and gilatoxin. [1]

下巴兩側有毒腺 

Common name / Trade name

-  Gila monster    

- Heloderma suspectum

- 希拉毒蜥

- The kallikrein-like activity of Heloderma venom is inhibited by carbon monoxide [2]

 

Involving SYSTEM

 

-          most (79%) occurred in males [3].  

-          Airway, angioedema. [4].

-          GI, diarrhea, nausea, vomiting [4, 5].

-          CV, hypotension, cardiac ischemia. [4]

-          Systemic, pain, diaphoresis. [1]

 

Presentation

 

-angioedema which can lead to respiratory tract obstruction [4]

-significant fluid losses due to diarrhea, vomiting, and sweating, associated with hypokalemia and sometimes metabolic acidosis [4, 5]

- atrioventricular conduction disorders simulating cardiac ischemia [4]

- hypotensive, and in shock [1, 5]

- atrial fibrillation requiring electrical cardioversion [5]

- pain, edema, nausea, vomiting, weakness, and diaphoresis. [1]

 

Antidote / Treatment

 

-There is no antivenom [1, 4]

-the treatment is only symptomatic and supportive. [4]

- Cryotherapy, tourniquet, and excision are dangerous and should not be used [1].

 

 

Disposition

- at least 6 hours of observation after the bite to assess [6]

- Majority of cases did not require hospitalization. [3]

- Heloderma bite are quite rare and generally mild. Few severe cases may require emergency resuscitation [4].

- (51%) were discharged home.

- (24%) were ED observation

-  15.6% admissions to an intensive care unit (ICU) [3].

-  Mortality rate: 0% till June 2024, not yet fatal report on PubMed. [3]

 

REFERENCES

 

1.      Strimple PD, Tomassoni AJ, Otten EJ, Bahner D. Report on envenomation by a Gila monster (Heloderma suspectum) with a discussion of venom apparatus, clinical findings, and treatment. Wilderness Environ Med. 1997 May;8(2):111-6. doi: 10.1580/1080-6032(1997)008[0111:roebag]2.3.co;2. PMID: 11990142.

2.      Nielsen VG, Frank N. The kallikrein-like activity of Heloderma venom is inhibited by carbon monoxide. J Thromb Thrombolysis. 2019 May;47(4):533-539. doi: 10.1007/s11239-019-01853-6. PMID: 30955141.

3.      French R, Brooks D, Ruha AM, Shirazi F, Chase P, Boesen K, Walter F. Gila monster (Heloderma suspectum) envenomation: Descriptive analysis of calls to United States Poison Centers with focus on Arizona cases. Clin Toxicol (Phila). 2015 Jan;53(1):60-70. doi: 10.3109/15563650.2014.988791. Epub 2014 Dec 16. PMID: 25511795.

4.      Chippaux JP, Amri K. Severe Heloderma spp. envenomation: a review of the literature. Clin Toxicol (Phila). 2021 Mar;59(3):179-184. doi: 10.1080/15563650.2020.1853145. Epub 2020 Dec 2. PMID: 33263449.

5.      Amri K, Chippaux JP. Report of a severe Heloderma suspectum envenomation. Clin Toxicol (Phila). 2021 Apr;59(4):343-346. doi: 10.1080/15563650.2020.1804574. Epub 2020 Aug 7. PMID: 32762570.

6.      Hooker KR, Caravati EM, Hartsell SC. Gila monster envenomation. Ann Emerg Med. 1994 Oct;24(4):731-5. doi: 10.1016/s0196-0644(94)70285-3. Erratum in: Ann Emerg Med 1995 Jan;25(1):47. PMID: 8092603.

 

14 July, 2024 edited by Yu-Jang Su

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

 

Lophophora williamsii Poisoning

 

 Substance

Lophophora williamsii, contains active alkaloids—such as pellotine, anhalonidine, hordenine and mescaline [1].

Plant: peyote [2]

less potent than LSD. [3, 4]

 

Common name or Trade name 

烏羽玉

 

Involving system

-       a serotonin agonist. [3]

-       serotonin 5HT2A/2C receptor agonist [4]

-       α1A/2A noradrenaline and D1/2/3 dopamine receptors.[4]

-       Toxidrome of a sympathomimetic effect. [5]

 

Presentation

Onset 30-60 minutes, lasts 5-12 hours (though wide individual variability) [3]

Psycho- Hallucination, agitation, euphoria, altered sensorium, altered sense of time, extreme focus or distractibility, hallucinations, Dizziness, headache. [3, 4] depersonalization and psychoses.[5]

CV- tachycardia, hypertension and vomiting. [3]

Abdomen - Nausea/vomiting, abdominal pain. [3]

Pupil - mydriasis [3]

Other - energy, esoteric/spiritual experiences. [3].

 

Antidote and Treatment

No antidote, standardly supportive treatment. [3]

Supportive care. [3]

Not usually associated with significant morbidity/mortality. [3]

 

Disposition

 Treat and observe.

 

References

[1]: Doesburg-van Kleffens M, Zimmermann-Klemd AM, Gründemann C. An Overview on the Hallucinogenic Peyote and Its Alkaloid Mescaline: The Importance of Context, Ceremony and Culture. Molecules. 2023 Dec 5;28(24):7942.

[2]:  Kapadia GJ, Highet RJ. Peyote alkaloids. IV. Structure of peyonine, novel beta-phenethylpyrrole from Lophophora williamsii. J Pharm Sci. 1968 Jan;57(1):191-2.

[3]. https://wikem.org/wiki/Mescaline_toxicity

[4]. Vamvakopoulou IA, Narine KAD, Campbell I, Dyck JRB, Nutt DJ. Mescaline: The forgotten psychedelic. Neuropharmacology. 2023 Jan 1;222:109294.

[5] Dinis-Oliveira RJ, Pereira CL, da Silva DD. Pharmacokinetic and Pharmacodynamic Aspects of Peyote and Mescaline: Clinical and Forensic Repercussions. Curr Mol Pharmacol. 2019;12(3):184-194.

Edited by Yu-Jang Su 

 21 May 2024

 

Bongkrekic Acid Poisoning

 

SUBSTANCE

  Bongkrekic acid

-          molecular weight of 486 kDa [1]    

-          ever been reported from Indonesia, China, and more recently in Mozambique.[1]

-          test liquid chromatography-tandem mass spectrometry (HPLC-MS/MS) using blood samples. [2].

-          B. cocovenenans is often called Pseudomonas cocovenenans subsp. farinofermentans. [3].

 

 

Common name / Trade name

-          Pathogenic bacteria Burkholderia gladiolus (B. gladiolus) foodborne. Burkholderia cocovenenans [4, 5]

-          Possible related food not well- reserved : wet rice and starch products, Tremella, and Auricularia auricula [6]    

-          Wet rice noodles with 4% soybean oil had a BA concentration of 31.72 ± 9.41 mg/kg, 5.74 times higher than those without soybean oil (5.53 ± 1.23 mg/kg). [6]

-          Mitochondrial toxins: it inhibits adenine nucleotide translocase (ANT)[1]

-          Not-well reserved coconut- or corn-based foods [1]

 

 

Involving SYSTEM

-          Liver :progressive dysfunction of liver function and coagulation function [3]

-      Kidney: Acute kidney injury.  [3]

-          Diffuse changes in the liver, hepatic failure. [3]

-          Brain, CNS.: Collapse and altered mental status.

 

Presentation

-          Altered mental status.

-          Hepatic failure.

-          Acute kidney injury

-          Shock presentation.

-          Collapse, sudden.

-          OHCA, (Out of Hospital Cardiac Arrest).

-          Respiratory failure.

-          Abdominal pain, diarrhea, vomiting, and generalized malaise. [7]

-          Death was preceded by psycho-motor agitation and abnormal posturing.[7]

 

 

Antidote / Treatment

- No specific antidote.

- Fresh frozen plasma.

- Plasma exchange was suggested. [8]

- Molecular Adsorbent Recirculating System (MARS) [9]

- Continuous veno-venous hemodiafiltration (CVVHDF)

- aggressive supportive care.

- ICU, intensive care is mandatory.

 

 

Disposition

 

-          mortality rate of up to 40 % or more [4]

-          The reported case fatality rates averaged 60%, 32%, and 26.5% [3]

-          The median course of disease in 9 cases was 53 hours (range: 20–341 hours).

-          In China a patient had the longest latency period, and he returned home after receiving prescription medication from the OPD. He then died at home with the shortest course of illness, which was only 20 hours. [3]

 

 

REFERENCES

 

[1] Anwar M, Kasper A, Steck AR, Schier JG. Bongkrekic Acid-a Review of a Lesser-Known Mitochondrial Toxin. J Med Toxicol. 2017 Jun;13(2):173-179. doi: 10.1007/s13181-016-0577-1.

 

[2]. Zhou B, Li HL, Ma J, Dong F, Yu Y. [Fast determination of bongkrekic acid in plasma by high performance liquid chromatography-tandem mass spectrometry]. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2022 Mar 20;40(3):219-221.

 

[3]. Yuan Y, Gao R, Liang Q, Song L, Huang J, Lang N, Zhou J. A Foodborne Bongkrekic Acid Poisoning Incident - Heilongjiang Province, 2020. China CDC Wkly. 2020 Dec 18;2(51):975-978.

 

[4] Wang T, Cheng B, Jiao R, Zhang X, Zhang D, Cheng X, Ling N, Ye Y. Characterization of a novel high-efficiency cracking Burkholderia gladiolus phage vB_BglM_WTB and its application in black fungus. Int J Food Microbiol. 2024 Apr 2;414:110615. doi: 10.1016/j.ijfoodmicro.2024.110615. Epub 2024 Feb 3. PMID: 38325260.

 

[5] Jiao Z, Kawamura Y, Mishima N, Yang R, Li N, Liu X, Ezaki T. Need to differentiate lethal toxin-producing strains of Burkholderia gladioli, which cause severe food poisoning: description of B. gladioli pathovar cocovenenans and an emended description of B. gladioli. Microbiol Immunol. 2003;47(12):915-25.

 

[6]. Yao Y, Zhong X, Zhou Y, Zhang H, Zhao D, Zhang W, Liu Y, Xu J, Xie C, Yu C, Wang Y, Chen Z, Chen K, Yuan J. Exploring the characteristics of Burkholderia gladioli pathovar cocovenenans: Growth, bongkrekic acid production, and potential risks of food contamination in wet rice noodles and vermicelli. Food Microbiol. 2024 Jun;120:104449.

 

[7]. Gudo ES, Cook K, Kasper AM, Vergara A, Salomão C, Oliveira F, Ismael H, Saeze C, Mosse C, Fernandes Q, Viegas SO, Baltazar CS, Doyle TJ, Yard E, Steck A, Serret M, Falconer TM, Kern SE, Brzezinski JL, Turner JA, Boyd BL, Jani IV; Chitima Investigation Group. Description of a Mass Poisoning in a Rural District in Mozambique: The First Documented Bongkrekic Acid Poisoning in Africa. Clin Infect Dis. 2018 Apr 17;66(9):1400-1406.

 

[8] Lv R, Zeng W, Zhang P, Chen X, Yuan K, Shen H, Tian J, Li D, Zhao L, Liu Y. The toxicokinetic and extracorporeal removal of bongkrekic acid during blood purification therapies: A case report. Toxicon. 2023 Sep;233:107275.

 

[9]. Saliba F. The Molecular Adsorbent Recirculating System (MARS) in the intensive care unit: a rescue therapy for patients with hepatic failure. Crit Care. 2006 Feb;10(1):118.

 

 

Edited by Yu-Jang Su         April 4, 2024