全氟和多氟烷基物質, Polyfluoroalkyl Substances, PFAS

 

Substance

PFAS（Per- and Polyfluoroalkyl Substances）[1].

一大類人工合成含氟有機化合物，具高度化學穩定性與生物累積性

常見代表：PFOA（Perfluorooctanoic acid）,PFOS（Perfluorooctane sulfonate）[1]

 

Common Name（常見名稱）

 

全氟／多氟烷基物質

永久化學物（Forever chemicals）

防水、防油、防污塗層化學品 [2]

列管物質：台灣已將 PFOA、PFOS、LPOS、POSF、PFHxS 等列為毒性或關注化學物質，有條件開放用途，如半導體、特定紡織品、滅火器等。

廣泛存在：市面上仍有許多未列管的PFAS種類流通，用於食品包裝、紡織品、化妝品、工業用途等，因其防水、防油特性。

台灣市售的許多隱形眼鏡都可能含有PFAS（全氟/多氟烷基物質）這類有機氟化物，主要用於提升鏡片光滑度、防止蛋白附著; 雖然專家認為從眼球進入體內的機會不大且致癌性未定，台灣消費者不必過度恐慌，但應關注,並追蹤 國際研究及美國 FDA 等單位對安全性的認定

 

Involving System（影響系統）

 

Multisystem, predominantly chronic effects

Liver: Elevated liver enzymes and hepatic steatosis [1]

Endocrine/Metabolic: Thyroid dysfunction and dyslipidemia [3] [4]

Immune system: Reduced vaccine antibody responses and immunosuppression [5]

Reproductive and developmental: Infertility, low birth weight, and developmental delay

                      increased FSH and decreased AMH, estradiol, and progesterone. [6]

Kidneys: Increased risk of chronic kidney disease [7].

Cardiovascular: Hypercholesterolemia and increased risk of atherosclerosis [4]

 

 

Presentation（臨床表現）

 

Acute exposure:

Mostly no obvious acute symptoms

Chronic exposure (common):

Asymptomatic with laboratory abnormalities:

ALT / AST ↑ [1]

Long-term epidemiological associations:

Metabolic syndrome [8]

Chronic kidney disease (CKD)[8]

Impaired immune function [5]

 

Antidote（解毒劑）

 

No specific antidote

Management principles:

Cessation of exposure (most important)

Supportive care

Investigational strategies (non-standard treatments):

Cholestyramine / bile acid sequestrants: may enhance elimination via interruption of Cholestyramine treatment led to a 23.1-fold increase in serum-adjusted fecal PFOS excretion. [9], 1 week 1 pack qd-bid ac

Over a 12-week period, colesevelam intervention reduced serum PFOS levels by an average of 38%, significantly outperforming the 2% decline observed in the control group [9]

Hemodialysis: does not work (largely ineffective for PFAS due to high protein binding)

 

Disposition（處置與去向）

                  Emergency department:

o    Asymptomatic or mildly symptomatic → outpatient follow-up

o    Routine hospitalization or gastric lavage is not required

Outpatient care / follow-up:

o    For individuals with occupational or environmental exposure:

§  Regular monitoring of:

§  Liver function

§  Lipid profile

§  Thyroid function

§  Renal function

o    Notify environmental or occupational medicine authorities (e.g., in cases of clustered exposure)

 

References

[1]. https://pubmed.ncbi.nlm.nih.gov/41543329/

[2]. https://pubmed.ncbi.nlm.nih.gov/41181096/

[3]. https://pubmed.ncbi.nlm.nih.gov/41391234/

[4]. https://pubmed.ncbi.nlm.nih.gov/41428216/

[5]. https://pubmed.ncbi.nlm.nih.gov/41456666/

[6]. https://pubmed.ncbi.nlm.nih.gov/41465861/

[7]. https://pubmed.ncbi.nlm.nih.gov/41440749/

[8]. https://pubmed.ncbi.nlm.nih.gov/40609416/

[9]. https://pubmed.ncbi.nlm.nih.gov/40974835/

Edited by Yu-Jang Su   Jan 17, 2026  

 

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 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]

• Feeling of inebriation or drunkenness.
• Headache, dizziness, and lethargy.
• Confusion, drowsiness, and ataxia (lack of coordination).
• Severe Cases: Stupor, coma, and respiratory arrest.

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

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。

本課程特別從天花、炭疽、新興病毒、肉毒桿菌毒素 等主題，邀集院內急診毒物與災難醫學學者與資深主治醫師，探討生物恐攻的防範、偵測、臨床處置與復原流程, 若真的發生了, 該採取什麼治療方式與用藥解危 。期盼歡迎大家參加，不僅增進大家的專業知識，也強化醫療體系面對新興生物威脅的整備韌性。課程全程免費，並申請多項專業學分，(已申請急診醫學會積分5分) https://www.sem.org.tw/Activity/B/Details/32259 , 誠摯邀請醫療同仁與公共衛生專業夥伴參與，共同守護國家生物安全.

報名費用：免費　　　　　　　        

報名方式：線上報名

報名網址：https://docs.google.com/forms/d/e/1FAIpQLSeN5ZrpGLAZIwIFiOLU5jSyxKNi27PrJKb2xwweyGd55i8T4w/viewform?pli=1

Edited by Yu-Jang Su  Nov 4, 2025.

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  

Toxic Substances Leading to Diarrhea

 

• • Heavy Metals / Environmental Pollutants / poisoning
  • Arsenic [1], lead [2], cadmium [3], mercury [4]
  • Mechanism: Disrupt intestinal epithelial barrier, induce inflammation, alter gut microbiota → electrolyte and fluid imbalance.
  • Chronic exposure common in children; environmental exposure is a major risk
  • Bacterial Enterotoxins /  Toxin 
  • Bacillus cereus (Nhe, Hbl, cereulide toxins) [5]
  • Clostridium perfringens enterotoxin [6]
  • Staphylococcus aureus enterotoxin [7].
  • Bongkrekic Acid Poisoning: 原名 米酵菌酸. https://twmmhedpc.blogspot.com/2024/04/bongkrekic-acid-poisoning.html
  • Mechanism: Toxins stimulate intestinal fluid secretion or damage intestinal lining
  • Presentation: Acute watery diarrhea, usually without blood or high fever
  • Marine Toxins
  • Diarrheic shellfish poisoning (okadaic acid) [8].
  • Ciguatera poisoning [9]
  • Presentation: Onset within a few hours after ingestion; symptoms include nausea, vomiting, abdominal pain, diarrhea; usually lasts a few days
  • Drugs / Chemical Agents
  • Colchicine: Early hallmark symptoms include severe vomiting and diarrhea (sometimes bloody) [10].
  • Antibiotics: May induce Clostridioides difficile infection, causing pseudomembranous colitis [6].
  • Methanol Poisoning: https://twmmhedpc.blogspot.com/2020/11/substance-methanol-ch-3-oh-common-name.html
  • 硼砂Na2B4O5(OH)4·8H2O中毒; 硼酸 H3BO3中毒 https://twmmhedpc.blogspot.com/2022/12/na2b4o5oh48h2o-h3bo3.html
  • Outcome: May result in severe dehydration and systemic toxicity.

  Others:

  Bitten injury by Heloderma suspectum, 希拉毒蜥 咬傷https://twmmhedpc.blogspot.com/2024/07/heloderma-suspectum-envenomation.html

  馬纓丹: https://twmmhedpc.blogspot.com/2025/03/lantana-camara-poisoning-intoxication.html

  雞母珠  Abrin : https://twmmhedpc.blogspot.com/2024/01/abrin-poisoning.html

   

  References

  [1]. https://pubmed.ncbi.nlm.nih.gov/36110556/   

  [2]. https://pubmed.ncbi.nlm.nih.gov/10810333/

  [3]. https://pubmed.ncbi.nlm.nih.gov/39619770/

  [4]. https://pubmed.ncbi.nlm.nih.gov/38613952/

  [5]. https://pubmed.ncbi.nlm.nih.gov/40695763/

  [6]. https://pubmed.ncbi.nlm.nih.gov/40625918/

  [7]. https://pubmed.ncbi.nlm.nih.gov/40679190/

  [8]. https://pubmed.ncbi.nlm.nih.gov/40819404/

  [9]. https://pubmed.ncbi.nlm.nih.gov/10081289/  

  [10]. https://pubmed.ncbi.nlm.nih.gov/38947441/

   

  Edited by Yu-Jang Su, September 17, 2025