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.

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🔹 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]

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🔹 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

   

   

   

  
  

Corrosive / Caustic Injury — Acids vs. Alkalis

 

Substances & Common Names

• Acids (酸)
• 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 (鹼)
• 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].

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Involving Systems

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

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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]

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Antidote

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

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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)

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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

•  

Giant Hogweed: An Invasive Threat to Health and Environment

  News 

Substance The primary hazard associated with giant hogweed lies in its sap, which contains furocoumarins or psoralens[1]. These phototoxic compounds are found throughout the plant, with the highest concentrations notably present in its fruits, leaves, and stem[1].

Importantly, the sap can retain its toxicity on exposed clothing for several hours after contact[1]. The concentration of these phototoxic compounds in giant hogweed is highest during the months of June, July, and August, aligning with periods of increased outdoor human activity[1].

 

Common Name Giant hogweed (Heracleum mantegazzianum) is a highly invasive flowering weed

Massive Size: A towering monocarpic perennial, reaching 3–5.5 meters tall with large leaves and white umbrella-shaped flowers.
[1][2] 

Origin & Spread: Native to the Caucasus, introduced to the UK in the 19th century, and later spread across Europe, the U.S. (1917), and Canada (1949).
[1][2]

Invasive Status: Listed as an invasive alien species of Union concern; ranked 22nd among Europe’s top 149 invasive species.
[2]

Habitat Range: Thrives in diverse areas—riversides, roadsides, fields, and even seashores—due to high adaptability.
[1][2]

Czech Distribution Example:In the Czech Republic, 84.7% grow in fields, 13.7% in forests, and just 1.6% in urban areas.
[2]

 

Involving System Contact with giant hogweed sap primarily affects the following systems:

●     Skin: Leading to a severe inflammatory reaction known as photophytodermatitis[1][2]. This is a non-immunologic form of dermatitis[1].[3]

●     Eyes: Direct eye contact with the sap can result in blindness[1][2].

●     Respiratory System: Inhalation of plant traces may cause obstructive pulmonary symptoms[1].

Presentations

Photophytodermatitis is triggered when UVA light activates furocoumarins (psoralens) in the plant sap, producing reactive oxygen species and DNA intercalation, leading to cell death and impaired healing [2]. Symptoms may begin within 15 minutes of exposure, with visible signs like erythema and edema typically appearing after 24 hours and peaking at 72 hours [1][2].

Skin injury ranges from mild redness to full-thickness chemical burns requiring debridement and grafting [1][2][4]. Severity increases with greater sap contact, sun exposure, humidity, heat, infection, and lack of protective clothing. Long-term hyperpigmentation can persist for weeks [1].

Photodistribution and Case Example:
The rash mainly appears on sun-exposed skin [2]. A 27-year-old landscaper trimming tall giant hogweed without protection developed severe blistering on his arms and neck, including large bullae (3–4 cm) and marked edema; his coworkers had milder reactions [1].

 

Antidote/Treatment

Effective management of giant hogweed exposure involves immediate action and symptomatic treatment:

●     Immediate Response: Upon contact with giant hogweed, it is crucial to immediately avoid any further UV exposure[1]. The affected area should be thoroughly rinsed with soap and water[1][2]. It is imperative to avoid UV radiation for at least 48 hours following exposure[1].

●     Topical Treatment: For mild reddening or erythema, a topical steroid can be applied to the affected area[1].

●     Pain Management: Pain can be alleviated by using a nonsteroidal anti-inflammatory drug[1].

●     Blister Management:

○     Small blisters can be carefully punctured and drained[1].

○     However, for large blisters, extensive epidermal-dermal separation, or large areas of detached epidermis, the recommendation is to simply cleanse and dress the affected area without puncturing[1].

●     Systemic Treatment: In cases of moderate to severe inflammation, an oral steroid may be prescribed. For instance, a patient was successfully treated with oral prednisone 70 mg daily (1 mg/kg/d), with the dosage gradually decreased by 10 mg every three days until the course was complete[1].

●     Surgical Intervention: Full-thickness chemical burns may necessitate surgical debridement and skin grafting[1].[5]

●     Post-Treatment Care: To manage open areas, mupirocin ointment can be applied, while petroleum jelly is recommended for intact skin[1]. Patients are also advised to practice strict photoprotection for both the immediate and long-term future[1].

Disposition

The prognosis for giant hogweed phytophotodermatitis, with appropriate treatment, can be favorable. In one clinical case, the severe phytophotodermatitis dramatically improved within several days, with complete resolution observed in one week. Postinflammatory hyperpigmentation, a common sequela, resolved after several weeks[1].

However, the broader implications of giant hogweed extend beyond individual health outcomes, encompassing significant economic and public health impacts across regions[1][2].

Public Health Impacts:

 

●     The large size and "charismatic" nature of the plant make it particularly dangerous for unsuspecting visitors or tourists, contributing to the risk of injury. Dense populations can physically impede access to valued amenity areas and reduce visibility along roadsides[2].

Management and Prevention Strategies:

Due to the phototoxicity of giant hogweed sap, control requires trained personnel with protective gear [1]. The plant is extremely invasive, producing up to 50,000 seeds per plant with a ~90% germination rate, making eradication long-term and resource-intensive [2]. Misidentification with native plants like Angelica or wild parsnip complicates detection [2]. In high-traffic areas, authorities may need to restrict public access to reduce human contact risk [2].

Although giant hogweed’s spread in North America has been relatively slow, European cases show that delayed action can lead to exponential invasion, escalating both health and economic impacts [1]. Early detection and rapid response are essential for cost-effective control. Regions bordering known invasion zones (e.g., Kentucky, Missouri, Tennessee) and underreported areas (e.g., New Hampshire) should stay vigilant to prevent widespread establishment [2].

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References

1. Cuddington K, Sobek-Swant S, Drake J, Lee W, Brook M. Risks of giant hogweed (Heracleum mantegazzianum) range increase in North America. Biol Invasions. 2022;24:299–314.
2. Flanagan KE, Blankenship K, Houk L. Botanical Briefs: Phytophotodermatitis Caused by Giant Hogweed (Heracleum mantegazzianum). Cutis. 2021;108:251-253.
3. Lagey K, Duinslaeger L, Vanderkelen A. Burns induced by plants. Burns. 1995 Nov;21(7):542-3. doi: 10.1016/0305-4179(95)00026-8. PMID: 8540985.
4. .Chan JC, Sullivan PJ, O'Sullivan MJ, Eadie PA. Full thickness burn caused by exposure to giant hogweed: delayed presentation, histological features and surgical management. J Plast Reconstr Aesthet Surg. 2011 Jan;64(1):128-30. doi: 10.1016/j.bjps.2010.03.030. Epub 2010 Apr 15. PMID: 20399165.
5. Baker BG, Bedford J, Kanitkar S. Keeping pace with the media; Giant Hogweed burns - A case series and comprehensive review. Burns. 2017 Aug;43(5):933-938. doi: 10.1016/j.burns.2016.10.018. Epub 2016 Dec 29. PMID: 28041748

Edited by   Hsiu-Wu Yang and   Yu-Jang Su

July 6, 2025