2025年12月9日 星期二

Acetone poisoning

 

Substance

 

去光水的主要成分是揮發性有機溶劑,最常見的丙酮(Acetone) 甲苯(Toluene),用於溶解指甲油中的高分子聚合物。 市面上也有較溫和的無丙酮去光水,可能含有乙醇(Ethanol)、醋酸乙酯(Ethyl Acetate)、異丙醇(Isopropyl Alcohol) , 醋酸丁酯 (Butyl acetate)或是添加大豆油酸甲酯等滋潤成分。 選擇時應注意標示,避免含有禁用的甲醇,並在通風處使用。 常用成分

丙酮(Acetone): 最常見的溶劑,溶解力強,但也容易使指甲乾燥、脆弱。

甲苯(Toluene): 也是常用成分,具有揮發性,但對健康影響較大。

醋酸乙酯(Ethyl Acetate): 另一種常見的有機溶劑。

異丙醇(Isopropyl Alcohol): 常用於無丙酮配方中。

 

Common name

去光水、卸甲液、洗甲水、除甲水。

英文名:Nail Polish Remover[1] CH3COCH3 [2]

 

 

Involving systems

Acetone:  metabolism of acetone is independent of the route of absorption and occurs primarily in the liver [1] excreted through the lung and a little through the urine irrespective of the route of exposure, and elimination is usually completed within 48-72 hours after exposure.

Central Nervous System (CNS): Primary target system. [3, 4]

Respiratory System: Mucous membrane irritation and potential respiratory depression.[3, 4]

Gastrointestinal (GI) System: Direct mucosal irritation. Vomiting, abdominal pain and gastrointestinal bleeding.[1]

Cardiovascular System: Potential for hypotension and tachycardia.[1]

Dermal/Ocular: Local irritant effects.[4]

 

 

Presentation

CNS Effects (Dose-dependent) [3]

Respiratory Effects [3]

  • Irritation of the nose, throat, and lungs. Bronchial edema [1]
  • Coughing and dyspnea (shortness of breath).
  • Hypoventilation (decreased respiratory rate).
  • Risk of aspiration pneumonitis if vomiting occurs.

GI Effects [1]

  • Nausea and vomiting.
  • Abdominal pain.
  • Sweet, fruity odor on the breath (characteristic of acetone).

Cardiovascular Effects

  • Hypotension (low blood pressure).[1]
  • Tachycardia (fast heart rate).[1]

Local Effects (Skin/Eyes)

  • Ocular: Eye irritation, pain, redness, and tearing. Corneal injury [4]
  • Dermal: Skin drying, cracking, and redness upon prolonged contact.

 

 

Antidote and Management

  • Supportive Care is Paramount: Focus on Airway, Breathing, and Circulation (ABC). [1]
  • Airway and Breathing: [1]
    • Monitor oxygen saturation and respiratory function closely.
    • Administer supplemental oxygen as needed.
    • Intubation and mechanical ventilation may be required for severe respiratory depression or failure.
  • Circulation:
    • Establish intravenous access (IV access).[1]
    • Administer IV fluids to manage hypotension.
    • Monitor ECG.
  • Decontamination (Ingestion):
    • DO NOT induce vomiting (risk of aspiration).
    • Gastric lavage is generally discouraged and rarely necessary, but may be considered for massive ingestion if performed early and with a protected airway.
    • Activated charcoal is ineffective against acetone.
  • Specific Monitoring:
    • Monitor acetone and serum ketone levels.
    • Monitor fluid and electrolyte status.
  • No Specific Antidote Exists.

 

 

Disposition

  • Mild to Moderate Exposure: Patients typically recover completely within hours to days, as acetone is relatively quickly metabolized and excreted.
  • Severe Intoxication: Prognosis depends on the severity and duration of CNS and respiratory depression.
    • Patients surviving the initial 48 hours generally have a favorable outcome.
    • Death is rare but can occur due to profound respiratory failure or aspiration pneumonitis.

For blood acetone levels of 20-30 mg/dl (severe intoxication), symptoms such as somnolence (drowsiness), ataxia (lack of coordination), slurred speech, and potentially deep coma may occur. A blood level of 55 mg/dl or higher is often considered the fatal level, based on concentrations detected in documented fatal poisoning cases. [1]

LD50:  oral LD50 value of 3,687 mg/kg was found for male guinea pigs (Strieger and Carpenter 1961). [4]

  • Discharge Criteria: Patients can typically be discharged once symptoms (especially CNS depression) have fully resolved and they are observed for a period of 4–6 hours post-exposure (depending on the dose and route). 

 

 

References

1.      https://pubmed.ncbi.nlm.nih.gov/34754632/,

2.      https://www.ncbi.nlm.nih.gov/books/NBK208291/

3.      https://pubmed.ncbi.nlm.nih.gov/3362729/

4.      https://www.ncbi.nlm.nih.gov/books/NBK590392/

 

Edited by Yu-Jang Su  Dec 9, 2025

2025年11月4日 星期二

活動訊息: 生物恐攻應變課程

面對全球公共衛生威脅與恐攻風險,我們醫療體系的前線應變能力與跨領域合作,顯得格外重要。

回顧歷史,2001年美國「Dark Winter」模擬演習以天花病毒為題,模擬大規模生物恐攻的社會影響。演練顯示,疫情一旦擴散,醫療與行政體系將在短時間內陷入混亂。三個月內,真實的「炭疽信件攻擊事件」隨即發生,造成5人死亡、17人感染,成為近代最著名的生物恐攻案例之一,也揭示了「模擬演習」可能成為現實預警的殘酷事實。

然而在2024年台北的BKA事件(Bongkrekic acid poisoning)中,雖非人為恐攻,但由於食物中毒症狀嚴重、毒理機轉複雜、早期難以診斷,導致群聚中毒與社會恐慌,顯示生物與化學毒素威脅在現代社會仍可能引發大規模公共衛生危機。

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Edited by Yu-Jang Su  Nov 4, 2025.

2025年10月18日 星期六

Poisoning Induced Myoclonus

 

1. Definition and Clinical Description

  • Myoclonus refers to sudden, brief, involuntary muscle jerks caused by abnormal central nervous system excitation. Poisoning-induced myoclonus can be multifocal or generalized, irregular or rhythmic. [1]
  • It includes positive myoclonus (sudden contraction) and negative myoclonus (brief loss of tone, e.g., asterixis).[1]
  • It is often mistaken for tremor or clonus, but differs in rhythm, mechanism, and duration.Clonus is rhythmic and stretch-reflex–driven, usually sustained.
  • Myoclonus is irregular, brief (<100 ms), and cannot be voluntarily controlled.
  • Differential: Tremor is rhythmic and often partially suppressible.

🔹 2. Mechanisms in Toxicology

  • Loss of GABAergic inhibition
    • Many toxins block GABA_A or GABA_B receptors, leading to decreased CNS inhibition. Examples include β-lactam antibiotics, isoniazid, theophylline, caffeine, diphenhydramine, cyclobenzaprine, and TCAs.
    • Mechanism: reduced GABA activity increases neuronal excitability, resulting in myoclonus or seizures.
  • Serotonergic overactivity (serotonin syndrome) [2]
    • Caused by SSRIs, MAOIs, linezolid, meperidine, tramadol, or fentanyl.
    • Myoclonus (59.5%) appears with hyperreflexia, agitation, tremor, and diaphoresis.
  • Metabolic or toxic accumulation
    • Occurs in uremia, hepatic encephalopathy, or drug accumulation in renal or hepatic failure.
    • Common agents include cefepime [3] and morphine.[4]
  • Excess excitatory amino acids (glutamate pathway)
    • Some toxins enhance NMDA or AMPA receptor activity.
    • Examples include domoic acid and organophosphates. [5]
  • Opioid toxicity or withdrawal
    • Certain opioids (meperidine, tramadol, fentanyl, morphine) produce neurotoxic metabolites such as normeperidine.
    • Presents with multifocal myoclonus and altered mental status.

 

🔹 3. Common Poisons and Drugs Causing Myoclonus

  • Antibiotics: cefepime, ceftriaxone, penicillin G.
  • Antidepressants: SSRIs, MAOIs, TCAs.
  • Analgesics: tramadol, meperidine, fentanyl, morphine (via metabolites).
  • Stimulants: amphetamines, cocaine [6], theophylline, caffeine.
  • Others: isoniazid, lithium, baclofen withdrawal [7], organophosphates [5], heavy metals.

 

🔹 4. Diagnostic Clues

  • EEG may show diffuse cortical spikes or polyspike–wave discharges.
  • Clinical pattern shows abrupt, arrhythmic, and sometimes stimulus-sensitive jerks.[1]
  • Myoclonus differs from seizures by being briefer and often without loss of consciousness. Always consider drug exposure, renal or hepatic impairment, and polypharmacy / Poisoning.

🔹 5. Management

  • Identify and discontinue the offending toxin or drug.
  • Correct metabolic abnormalities such as uremia, hypoxia, or electrolyte imbalance.
  • Perform hemodialysis if due to a renally excreted neurotoxic agent (e.g., cefepime, lithium, isoniazid).
  • Use benzodiazepines (clonazepam, diazepam, lorazepam) to enhance GABAergic inhibition.[1]
  • Valproate or levetiracetam can be used in persistent cases.[1]
  • Avoid serotonergic or excitatory agents.
  • Cyproheptadine is useful for serotonin syndrome.
  • Pyridoxine (vitamin B6) should be given in isoniazid toxicity.[8]

🔹 6. Summary

Myoclonus is an important warning sign of neurotoxicity in poisoning. Always assess renal function and cumulative neurotoxic drug exposure. EEG monitoring helps identify subclinical epileptiform activity. Main management principle: stop the toxin and enhance GABAergic inhibition.

References

[1]. https://www.ncbi.nlm.nih.gov/books/NBK537015/

[2]https://pubmed.ncbi.nlm.nih.gov/31688388/

[3]https://pubmed.ncbi.nlm.nih.gov/39068595/

[4]. https://pubmed.ncbi.nlm.nih.gov/9204657/

[5]. https://pubmed.ncbi.nlm.nih.gov/36609395/

[6]. https://pubmed.ncbi.nlm.nih.gov/116267/

[7]. https://pubmed.ncbi.nlm.nih.gov/12736874/

[8].https://pubmed.ncbi.nlm.nih.gov/2796112/

 

 Edited by Yu-Jang Su Oct 18, 2025  

2025年9月17日 星期三

Toxic Substances Leading to Diarrhea

 


2025年8月21日 星期四

Corrosive / Caustic Injury — Acids vs. Alkalis

 

Substances & Common Names

  • Acids ()
    • Hydrochloric acid (鹽酸,除鏽劑、清潔劑)[1]
    • Sulfuric acid (硫酸,汽車電池液) [2]
    • Nitric acid (硝酸,肥料/工業)[3]
    • Hydrofluoric acid (氫氟酸,玻璃蝕刻、金屬清潔)[4]
  • Alkalis ()
    • Sodium hydroxide (氫氧化鈉/苛性鈉,水管疏通劑)[5].
    • Potassium hydroxide (氫氧化鉀,烤箱清潔劑)[6].
    • Calcium hydroxide (氫氧化鈣,石灰) [7].
    • Ammonia (氨水,清潔劑/工業) [8].
    • Sodium hypochlorite (次氯酸鈉,家用漂白水 3–6%) [9].

Involving Systems

  • 主要影響:GI tractairwayeyesskin [1], [5], [9]
  • → coagulative necrosis,表層壞死較多,但也可穿孔 [1]
  • → liquefactive necrosis,深層滲透壞死食管灼傷更嚴重 [10].

Presentation

  • 共同表現
    • 咽喉痛、流涎、吞嚥困難、嘔吐、胸/腹痛 [1]
    • 嚴重上消化道出血、穿孔、縱隔炎、呼吸困難 [1]
  • 酸特徵 (尤其 HF)
    • 胃為主要損傷部位 [1]
    • HF:低血鈣、心律不整、QT 延長 [4]
  • 鹼特徵
    • 深入食管高風險穿孔、狹窄 [6]
    • 常見氣道水腫、聲音沙啞、呼吸窘迫 [6]

Antidote

  • 一般酸/:無特效解毒劑[6]
  • HF 特例Calcium gluconate (IV topical gel) [4]

Disposition / Management [1, 4, 6]

  • Immediate
    • Airway first:出現聲音沙啞、喘鳴、流涎早期插管
    • 禁止催吐、洗胃、活性碳
    • 可給予牛奶/水少量稀釋 (非強制)
  • Evaluation
    • 12–24 小時內胃鏡檢查 (避免 >48 小時)
    • 影像檢查 (CT) 若懷疑穿孔
  • Treatment
    • Supportive care, IV fluids, pain control
    • 類固醇:具爭議,可能降低食管狹窄,但感染風險
    • 外科手術:穿孔、廣泛壞死時
  • Long-term
    • 食管狹窄 (最常見後遺症)
    • 增加食管癌風險 (特別是鹼灼傷)

References

  • [1].Yu CH, Su YJ, Lai YC. Fatal Zargar grade 3b corrosive injury after hydrochloric acid ingestion: A case report. Medicine (Baltimore). 2024 Oct 4;103(40):e40017. doi: 10.1097/MD.0000000000040017. PMID: 39465708; PMCID: PMC11460919.
  •  
  • [2]. Mastrodicasa E. Sulfuric Acid Ingestion: May the Severity of the Metabolic Acidosis be Considered as a Predictive Sign of Late Damage to the Gastrointestinal Tract? Eur J Case Rep Intern Med. 2024 Apr 9;11(5):004437. doi: 10.12890/2024_004437. PMID: 38715891; PMCID: PMC11073603.
  •  
  • [3]. Colalillo JM, Skinner K. Why so blue? A novel presentation of methaemoglobinaemia secondary to an inhaled occupational nitric acid exposure. Clin Toxicol (Phila). 2025 Feb;63(2):145-147. doi: 10.1080/15563650.2024.2440547. Epub 2024 Dec 18. PMID: 39692141.
  •  
  • [4].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. Erratum in: Am J Emerg Med. 2009 Jan;27(1):126. PMID: 11555812.
  •  
  • [5].Barnes SS, Wong W Jr, Affeldt JC. A case of severe airbag related ocular alkali injury. Hawaii J Med Public Health. 2012 Aug;71(8):229-31. PMID: 22900239; PMCID: PMC3419824.
  •  
  • [6].Chibishev A, Pereska Z, Chibisheva V, Simonovska N. Corrosive poisonings in adults. Mater Sociomed. 2012;24(2):125-30. doi: 10.5455/msm.2012.24.125-130. PMID: 23678319; PMCID: PMC3633385.
  •  
  • [7].Schmidt SM, Schmidt CJ, Adler M, Rahmani B. Corneal injury due to a calcium hydroxide containing food preparation product ("cal"). Pediatr Emerg Care. 2008 Jul;24(7):468-70. doi: 10.1097/PEC.0b013e31817de2d3. PMID: 18633308.
  •  
  • [8].Czerwiec A, Chevallier C, Grenet G, Patat AM, de Souza S, Lichtfouse J; French Poison Centres Research Group; Boucher A, Paret N; List of French Poison Centres (Centre antipoison). Exposure to ammonia solution due to substance use: a retrospective study from the French poison centres database (2009-2018). Clin Toxicol (Phila). 2024 Feb;62(2):107-111. doi: 10.1080/15563650.2024.2313088. Epub 2024 Feb 28. PMID: 38416057.
  •  
  • [9].Patterson J, Vallance V. Severe chemical pneumonitis following exposure to household bleach. BMJ Case Rep. 2025 Mar 27;18(3):e262924. doi: 10.1136/bcr-2024-262924. PMID: 40147947.
  •  
  • [10].Boonekamp C, Voruz F, Fehlmann C. Accidental aspiration of a solid tablet of sodium hydroxide. BMJ Case Rep. 2018 Jun 21;2018:bcr2018224213. doi: 10.1136/bcr-2018-224213. Erratum in: BMJ Case Rep. 2018 Aug 17;2018:bcr-2018-224213corr1. doi: 10.1136/bcr-2018-224213corr1. PMID: 29930183; PMCID: PMC6020962.

Edited by Yu-Jang Su       Aug 21, 2025
  •  

Acetone poisoning

  Substance   去光水的主要成分是揮發性有機溶劑,最常見的 丙酮 ( Acetone ) 和 甲苯 ( Toluene ) ,用於溶解指甲油中的高分子聚合物。 市面上也有較溫和的無丙酮去光水,可能含有 乙醇 (Ethanol) 、醋酸乙酯 ( Ethyl...