SalioSAM/toxsample11 huggingface dataset:
Poisoning cause: Severe morphine toxicity
Management: Administer oxygen and assist ventilation for respiratory depression. Naloxone is the antidote indicated for severe toxicity (respiratory or CNS depression). Orotracheal intubation for airway protection should be performed early in cases of obtundation and/or respiratory depression that do not respond to naloxone. NALOXONE, an opioid antagonist, is the specific antidote. Naloxone can be given intravascularly, intramuscularly, subcutaneously, intranasally or endotracheally. The usual dose is 0.4 to 2.0 mg IV. In patients with suspected opioid dependence, incremental doses of 0.2 mg IV should be administered, titrated to reversal of respiratory depression and coma, to avoid precipitating acute opioid withdrawal. Doses may be repeated every 2 to 3 minutes up to 20 mg, although such high doses are rarely needed
Clinical effect 1: Respiratory depression
Clinical effect 2: Respiratory arrest
Clinical effect 3: Hypoxia
Clinical effect 4: Coma
Clinical effect 5: Bradycardia
Clinical effect 6: Acute lung injury
Clinical effect 7: Seizure
Clinical effect 8: Hypoxia
Clinical effect 9: Death
Poisoning cause: Mild to moderate oxycodone poisoning
Toxic dose : Toxic Dose Threshold: ≥0.25 mg/kg for age 6 months - 79 years
Management: Patients may need only observation for CNS excitation or depression and respiratory depression
Clinical effect 1: Euphoria
Clinical effect 2: Drowsiness/lethargy
Clinical effect 3: Constipation
Clinical effect 4: Nausea
Clinical effect 5: Vomiting
Clinical effect 6: Abdominal pain
Clinical effect 7: Miosis
Clinical effect 8: Bradycardia
Clinical effect 9: Hypotension
Poisoning cause: Severe oxycodone poisoning
Toxic dose : Toxic Dose Threshold: ≥0.25 mg/kg for age 6 months - 79 years
Management: Administer oxygen and assist ventilation for respiratory depression. Naloxone is the antidote indicated for severe toxicity (respiratory or CNS depression). Orotracheal intubation for airway protection should be performed early in cases of obtundation and/or respiratory depression that do not respond to naloxone. NALOXONE, an opioid antagonist, is the specific antidote. Naloxone can be given intravascularly, intramuscularly, subcutaneously, intranasally or endotracheally. The usual dose is 0.4 to 2.0 mg IV. In patients with suspected opioid dependence, incremental doses of 0.2 mg IV should be administered, titrated to reversal of respiratory depression and coma, to avoid precipitating acute opioid withdrawal. Doses may be repeated every 2 to 3 minutes up to 20 mg, although such high doses are rarely needed
Clinical effect 1: Respiratory depression
Clinical effect 2: Respiratory arrest
Clinical effect 3: Hypoxia
Clinical effect 4: Coma
Clinical effect 5: Bradycardia
Clinical effect 6: QTc prolongation
Clinical effect 7: Acute lung injury
Clinical effect 8: Seizure
Clinical effect 9: Hypoxia
Clinical effect 10: Death
Poisoning cause: Mild to moderate fentanyl toxicity
Management: Patients may need only observation for CNS excitation or depression and respiratory depression
Clinical effect 1: Euphoria
Clinical effect 2: Drowsiness/lethargy
Clinical effect 3: Headache
Clinical effect 4: Anxiety
Clinical effect 5: Dizziness
Clinical effect 6: Constipation
Clinical effect 7: Nausea
Clinical effect 8: Vomiting
Clinical effect 9: Miosis.
Poisoning cause: Severe fentanyl poisoning
Management: Administer oxygen and assist ventilation for respiratory depression. Naloxone is the antidote indicated for severe toxicity (respiratory or CNS depression). Orotracheal intubation for airway protection should be performed early in cases of obtundation and/or respiratory depression that do not respond to naloxone. 
Clinical effect 1: Respiratory depression
Clinical effect 2: Respiratory arrest
Clinical effect 3: Hypoxia
Clinical effect 4: Hypotension
Clinical effect 5: Hypotension 
Clinical effect 6: Death
Poisoning cause: Mild to moderate methcathinone toxicity
Toxic dose : Acute ingestion of as little as 15–40 mg/kg can produce toxicity.
Management: Treatment is symptomatic and supportive; patients may only require observation. Benzodiazepines should be given for sedation as needed. Reassure the patient. Intravenous fluids and antiemetics may be indicated. 
Clinical effect 1: Agitation/Irritability/Restlessness
Clinical effect 2: Tachycardia
Clinical effect 3: Hypertension
Clinical effect 4: Mydriasis
Clinical effect 5: Insomnia
Clinical effect 6: Anorexia
Clinical effect 7: Hallucinations
Clinical effect 8: Paranoia
Clinical effect 9: Palpitations
Clinical effect 10: Psychosis
Poisoning cause: Severe methcathinone toxicity
Toxic dose : Severe toxicity is common after ingestion of 80–150 mg/kg.With chronic use, 10–20% of patients will develop hepatic toxicity when the dose is 10 mg/kg/day, but less than 2% will develop this toxicity if the dose is 3–5 mg/kg/day.
Older persons are more susceptible to chronic toxicity​​.
Management: Goal of therapy is to control agitation, reverse or prevent hyperthermia, and support the paranoid or delirious patient. Liberal use of benzodiazepines are the mainstay of therapy. Administer intravenous fluids. Orotracheal intubation is indicated for airway protection in cases of severe agitation, coma or recurrent seizure activity. Treatment is symptomatic and supportive. Provide a calm and supportive environment. Benzodiazepines should be given to treat delirium, seizures and moderate hypertension or tachycardia
Clinical effect 1: Agitated delirium
Clinical effect 2: Aggressive behavior
Clinical effect 3: Hallucinations
Clinical effect 4: Paranoia
Clinical effect 5: Hyperthermia
Clinical effect 6: Hypotension
Clinical effect 7: Rhabdomyolysis
Clinical effect 8: Renal failure
Clinical effect 9: Hyperkalemia
Clinical effect 10: Acidosis
Clinical effect 11: Cardiac dysrhythmias
Clinical effect 12: Elevated hepatic enzymes
Clinical effect 13: Coagulopathy
Clinical effect 14: Coma
Clinical effect 15: Seizure
Clinical effect 16: Dysrhythmias
Clinical effect 18: Vascular ischemia of the lower extremities
Poisoning cause: Lsd toxicity
Management: For mild to moderate toxicity, treatment is largely supportive. This includes the use of benzodiazepines, such as lorazepam or diazepam, for anxiety or agitation.
Clinical effect 1: Hallucinations
Clinical effect 2: Behavioral changes/Bizarre behavior / altered mentation
Clinical effect 3: Paranoia
Clinical effect 4: Mood fluctuations
Clinical effect 5: Acute psychotic reactions
Clinical effect 6: Tension
Clinical effect 7: Lightheadedness
Clinical effect 8: Mydriasis
Clinical effect 9: Twitching
Clinical effect 10: Flushing
Clinical effect 11: Tachycardia
Clinical effect 12: Hypertension
Clinical effect 13: Hyperreflexia
Clinical effect 14: Perceptual changes
Clinical effect 15: Euphoria
Clinical effect 16: Mood swings
Clinical effect 17: Depersonalization
Clinical effect 18: Derealization
Clinical effect 19: Loss of body image
Clinical effect 20: "flashbacks
Clinical effect 21: " panic reactions
Clinical effect 22: Seizure
Clinical effect 23: Rhabdomyolysis
Poisoning cause: Mild to moderate colchicine poisoning
Toxic dose : patients with colchicine overdose ingestions, ingestions of less than 0.5 mg/kg resulted in milder adverse reactions (eg, gastrointestinal effects), 
Management: Treatment is supportive with attention to the airway, breathing, and circulation. For mild to moderate Overdose, consider GI decontamination and treat for shock. Administer IV fluids, antiemetics, and pressors if needed.
Clinical effect 1: Nausea
Clinical effect 2: Vomiting
Clinical effect 3: Diarrhea
Clinical effect 4: Abdominal pain
Poisoning cause: Severe colchicine poisoning
Toxic dose : ingestions of 0.5 to 0.8 mg/kg developed more serious adverse reactions, including myelosuppression, and ingestions greater than 0.8 mg/kg resulted in 100% mortality.
Management: Treatment is supportive in the ICU. Multiorgan system failure may occur 1 to 7 days post-ingestion. Treat with IV fluids, vasopressors, cardiac monitoring, intubation, antibiotics for sepsis, dialysis for acute renal failure as needed. Pancytopenia has been reported. For severe neutropenia, administer colony stimulating factor (e.g., filgrastim, sargramostim). If severe coagulopathy with bleeding develops transfuse with RBCs, platelets and fresh frozen plasma as indicated. Treat seizures with IV benzodiazepines or barbiturates. Consider pacemaker insertion for high degree AV block.
Clinical effect 1: Nausea
Clinical effect 2: Vomiting
Clinical effect 3: Diarrhea (bloody)
Clinical effect 4: Abdominal pain
Clinical effect 5: Dehydration
Clinical effect 6: Leukocytosis
Clinical effect 7: Hypotension
Clinical effect 8: Dysrhythmias
Clinical effect 9: Confusion
Clinical effect 10: Coma
Clinical effect 11: Seizure
Clinical effect 12: Pancytopenia
Clinical effect 13: Renal failure
Clinical effect 14: Hepatic failure
Clinical effect 15: Sepsis
Clinical effect 16: Acute lung injury
Clinical effect 17: Electrolyte distrubances
Clinical effect 18: Rhabdomyolysis
Clinical effect 19: Alopecia
Clinical effect 20: Myopathy
Clinical effect 21: Neuropathy
Clinical effect 22: Myoneuropathy
Clinical effect 23: Death
Clinical effect 24: Respiratory depression
Clinical effect 25: Shock
Clinical effect 26: Dysrhythmias
Clinical effect 27: Cardiac arrest
Poisoning cause: Mild to moderate methadone toxicity
Toxic dose : >0 mg
Management: Symptomatic and supportive care with continuous monitoring of airway patency is the mainstay of treatment in patients who present with mild to moderate methadone toxicity. Carefully monitor respiratory rate and end tidal CO2 to avoid unrecognized respiratory depression.
Clinical effect 1: Lightheadedness
Clinical effect 2: Dizziness
Clinical effect 3: CNS depression
Clinical effect 4: Nausea
Clinical effect 5: Vomiting
Clinical effect 6: Miosis
Clinical effect 7: Constipation
Poisoning cause: Severe methadone toxicity
Toxic dose : >0 mg
Management: Administer oxygen and assist ventilation for respiratory depression. Naloxone is the antidote indicated for severe toxicity (respiratory or CNS depression). Early intubation and ventilation assistance should be performed if respiratory depression does not respond to naloxone. Adequate circulatory support with IV fluids and vasopressors (if needed) should be assured if a patient presents with circulatory collapse that does not reverse with naloxone. Treat seizures with benzodiazepines, propofol and/or barbiturates. Monitor for QT prolongation and dysrhythmias, and follow the appropriate ACLS algorithm if needed. Consider extracorporeal membrane oxygenation in cases of pulmonary edema not responsive to mechanical ventilation with high PEEP.
Clinical effect 1: Coma
Clinical effect 2: Respiratory depression
Clinical effect 3: Respiratory arrest
Clinical effect 4: Pulmonary edema
Clinical effect 5: Bradycardia
Clinical effect 6: Hypotension
Clinical effect 7: QTc prolongation
Clinical effect 8: Torsade de pointes
Clinical effect 9: Dysrhythmias
Clinical effect 10: Ventricular tachycardia
Clinical effect 11: Ventricular fibrillation
Clinical effect 12: Cardiomyopathy
Clinical effect 13: Syncope
Clinical effect 14: Rhabdomyolysis
Clinical effect 15: Seizure
Clinical effect 16: Cardiac arrest
Clinical effect 17: Death
Clinical effect 18: Hypoglycemia
Clinical effect 19: Nonketotic hyperglycemia
Poisoning cause: Mild to moderate organophosphate poisoning
Management: A patient who is either asymptomatic or presents with mild clinical symptoms (i.e. normal vitals, pulse oximetry and an acetylcholinesterase greater than 80% of lower reference range), and remains stable for 12 hours can be discharged. Obtain appropriate psychiatric evaluation if an intentional exposure. 
Clinical effect 1: Bradycardia
Clinical effect 2: Salivation
Clinical effect 3: Lacrimation
Clinical effect 4: Diaphoresis
Clinical effect 5: Vomiting
Clinical effect 6: Diarrhea
Clinical effect 7: Urination
Clinical effect 8: Miosis
Clinical effect 9: Tachycardia
Clinical effect 10: Hypertension
Clinical effect 11: Mydriasis
Clinical effect 12: Muscle cramps
Poisoning cause: Severe organophosphate poisoning
Management: Immediate assessment and evaluation. Airway management is likely to be necessary. Simple decontamination (i.e. skin and gastrointestinal, removal of contaminated clothes). Administer antidotes: atropine for muscarinic manifestations (e.g. salivation, diarrhea, bronchorrhea), pralidoxime for nicotinic manifestations (e.g. weakness, fasciculations). Treat seizures with benzodiazepines. Admit to intensive care with continuous monitoring, titration of antidotes, ventilation, and inotropes as needed. Consult a medical toxicologist and/or poison center. Organophosphates are highly lipid soluble. An 8-year-old boy with acute severe organophosphate poisoning was successfully treated with therapeutic plasma exchange, high-volume hemodiafiltration, and lipid infusion. Consider intravenous lipid therapy for patients with ventricular dysrhythmias or hypotension who do not respond to other therapies. 
Clinical effect 1: Bronchorrhea
Clinical effect 2: Bronchospasm
Clinical effect 3: Acute lung injury
Clinical effect 4: Muscle fasciculations
Clinical effect 5: Weakness
Clinical effect 6: Respiratory depression
Clinical effect 7: CNS depression
Clinical effect 8: Agitation/Irritability/Restlessness
Clinical effect 9: Confusion
Clinical effect 10: Delirium
Clinical effect 11: Coma
Clinical effect 12: Seizure
Clinical effect 13: Hypotension
Clinical effect 14: Ventricular dysrhythmias
Clinical effect 15: Acidosis
Clinical effect 16: Pancreatitis
Clinical effect 17: Hyperglycemia
Poisoning cause: MILD TO MODERATE Primidone TOXICITY
Toxic dose :  Ingestion of 8 mg/kg phenobarbital generally causes some CNS depression in non-tolerant individuals.Toxicity is likely when the dose exceeds 5–10 times the hypnotic dose. Per Olson guidleine:Acute ingestion of as little as 15-40 mg/kg can produce toxicity,
Toxic serum or urine levels: Phenobarbital levelsfrom 3 to 40 mcg/ml (lethargy and ataxia)
Management: Activated charcoal may be given if patients present shortly after ingestion, and are awake and alertwith a protected airway
Clinical effect 1: Drowsiness/lethargy
Clinical effect 2: Slurred speech
Clinical effect 3: Nystagmus
Clinical effect 4: Confusion
Clinical effect 5: Ataxia
Poisoning cause: SEVERE PrimidoneTOXICITY
Toxic dose :  Ingestion of 8 mg/kg phenobarbital generally causes some CNS depression in non-tolerant individuals.Toxicity is likely when the dose exceeds 5–10 times the hypnotic dose. Per Olson guidleine, severe toxicity is common after ingestion of 80-150 mg/kg. For chronic use, hepatic toxicity develops in 10-20% of patients when the daily dose is around 10 mg/kg, but this drops to less than 2% when the dose is between 3-5 mg/kg per day. Additionally, older individuals are more susceptible to chronic toxicity from Primidone​​.
Toxic serum or urine levels: Phenobarbital levels  from 60 to 150 mcg/ml (coma), above 150 mcg/ml (hypotension and coma)
Management: Orotracheal intubation for airway protection should be performed if patient is increasingly drowsy or comatose. Administer activated charcoal (GI decontamination should be performed only in patients who can protect their airway or who are intubated). Severe hypotension and hypothermia may develop; aggressive supportive care is the mainstay of treatment including passive rewarming, administration of normal saline, and in severe cases vasopressors. QT interval prolongation may occur with IV phenobarbital sodium administration. In patients with QT prolongation, monitor serum electrolytes including potassium, calcium and magnesium in patients with significant Overdose; correct any abnormalities. Concomitant use of IV phenobarbital sodium and other drugs that prolong the QT interval may increase the risk of torsades de pointes. Treat torsades de pointes with IV magnesium sulfate, and correct electrolyte abnormalities, Overdrive pacing may be necessary. At the time of this review, torsades de pointes has not been reported with therapy. Overall, clinical manifestations may be prolonged due to long half-life of drug. Tetanus and routine wound care for blisters. A burn surgeon should be consulted for extensive skin blistering
Clinical effect 1: Coma
Clinical effect 2: Hypotension
Clinical effect 3: Decreased myocardial contractility
Clinical effect 4: Hypothermia
Clinical effect 5: Respiratory depression
Clinical effect 6: Blisters
Clinical effect 7: Miosis
Clinical effect 8: Diminished reflexes
Clinical effect 9: Respiratory depression
Clinical effect 10: Cardiovascular collapse
Clinical effect 11: Aspiration pneumonia
Clinical effect 12: Rhabdomyolysis
Clinical effect 13: Renal failure
Poisoning cause: MILD TO MODERATE Zopiclone and eszopiclone TOXICITY
Toxic dose : 6 months - 23 months: A toxic dose of Zopiclone is considered to be greater than 2.5 mg. 2 years - 6 years: A toxic dose of Zopiclone is considered to be greater than 5 mg. 7 years - 17 years: A toxic doseof Zopiclone is is considered to be greater than 7.5 mg. 18 years - 64 years: A toxic doseof Zopiclone is is considered to be greater than 15 mg. 65 years - 79 years: A toxic doseof Zopiclone is considered to be greater than 7.5 mg.-----------6 months - 23 months: A toxic dose of Eszopiclone is considered to be greater than 1 mg.
2 years - 6 years: A toxic dose of Eszopiclone is considered to be greater than 2 mg.
7 years - 17 years: A toxic dose of Eszopiclone is considered to be greater than 4 mg.
18 years - 64 years: A toxic dose of Eszopiclone is considered to be greater than 6 mg.
65 years - 79 years: A toxic dose of Eszopiclone is considered to be greater than 4 mg.
Management: Most patients will require little more than monitoring and positioning to maintain the airway and avoid aspiration.
Clinical effect 1: drowsiness
Clinical effect 2: ataxia
Clinical effect 3: lethargy
Clinical effect 4: sedation
Poisoning cause: Severe Zopiclone and Eszopiclone Toxicity
Toxic dose : 6 months - 23 months: A toxic dose of Zopiclone is considered to be greater than 2.5 mg. 2 years - 6 years: A toxic dose of Zopiclone is considered to be greater than 5 mg. 7 years - 17 years: A toxic doseof Zopiclone is is considered to be greater than 7.5 mg. 18 years - 64 years: A toxic doseof Zopiclone is is considered to be greater than 15 mg. 65 years - 79 years: A toxic doseof Zopiclone is considered to be greater than 7.5 mg.-----------6 months - 23 months: A toxic dose of Eszopiclone is considered to be greater than 1 mg.
2 years - 6 years: A toxic dose of Eszopiclone is considered to be greater than 2 mg.
7 years - 17 years: A toxic dose of Eszopiclone is considered to be greater than 4 mg.
18 years - 64 years: A toxic dose of Eszopiclone is considered to be greater than 6 mg.
65 years - 79 years: A toxic dose of Eszopiclone is considered to be greater than 4 mg.
Poisoning cause: MILD TO MODERATE  tizanidine TOXICITY
Toxic dose : Based on the triage criteria you provided for Tizanidine ingestion, here’s how to assess the need for emergency room (ER) evaluation:
6 months to 23 months: Triage to the ER if the ingested amount is greater than 0.05 mg/kg OR more than 1 mg.
2 years to 6 years: Triage to the ER if the ingested amount is 4 mg or more.
7 years to 64 years: Triage to the ER if the ingested amount is 16 mg or more.
65 years to 79 years: Triage to the ER if the ingested amount is more than 8 mg
Management: There is no specific treatment. Monitor vital signs. Hypotension should be treated with intravenous fluids. Bradycardia is typically mild and usually does not require any treatment. Bradycardia, hypotension and CNS depression often respond to physical stimulation. Children (l6 years of age or less) may develop more anxiety and aggression following exposure; these patients may need a quiet and supportive environment.
Poisoning cause:   Severe tizanidine TOXICITY
Toxic dose : Based on the triage criteria you provided for Tizanidine ingestion, here’s how to assess the need for emergency room (ER) evaluation:
6 months to 23 months: Triage to the ER if the ingested amount is greater than 0.05 mg/kg OR more than 1 mg.
2 years to 6 years: Triage to the ER if the ingested amount is 4 mg or more.
7 years to 64 years: Triage to the ER if the ingested amount is 16 mg or more.
65 years to 79 years: Triage to the ER if the ingested amount is more than 8 mg
Management:  Severe bradycardia associated with hypotension that is not responsive to physical stimulation should be treated with a standard dose of atropine or cardiac pacing. Vasopressors (eg, norepinephrine) may be beneficial in patients with severe bradycardia and hypotension not responding to physical stimulation, naloxone, intravenous fluids and/or atropine. Patients with significant CNS and/or respiratory depression should be intubated.
Poisoning cause: MILD TO MODERATE armodafinil  TOXICITY
Toxic dose : 6 months - 5 years:	>150 mg,
6 years - 17 years:	>200 mg,
18 years - 64 years:	>450 mg,
65 years - 79 years:	>200 mg
Management: A) MANAGEMENT OF MILD TO MODERATE TOXICITY
1) Treatment is symptomatic and supportive.
Poisoning cause: SEVERE  armodafinil TOXICITY
Toxic dose : 6 months - 5 years:	>150 mg,
6 years - 17 years:	>200 mg,
18 years - 64 years:	>450 mg,
65 years - 79 years:	>200 mg
Management: MANAGEMENT OF SEVERE TOXICITY
1) Treatment is symptomatic and supportive. Monitor neurologic status. Alterations in heart rhythm and blood pressure may occur. Monitor vital signs. Obtain a baseline ECG and institute continuous cardiac monitoring in patients with tachycardia. Sinus tachycardia does not generally require treatment unless hemodynamic compromise is present. If therapy is required, a short-acting, cardioselective agent such as esmolol is generally preferred.
Poisoning cause: MILD TO MODERATE Modafinil  TOXICITY
Toxic dose : 6 months - 5 years:	>200 mg,
6 years - 17 years:	>300 mg,
18 years - 64 years:	>600 mg,
65 years - 79 years:	>300 mg
Management: A) MANAGEMENT OF MILD TO MODERATE TOXICITY
1) Treatment is symptomatic and supportive.
Poisoning cause: SEVERE Modafinil  TOXICITY
Toxic dose : 6 months - 5 years:	>200 mg,
6 years - 17 years:	>300 mg,
18 years - 64 years:	>600 mg,
65 years - 79 years:	>300 mg
Management: MANAGEMENT OF SEVERE TOXICITY
1) Treatment is symptomatic and supportive. Monitor neurologic status. Alterations in heart rhythm and blood pressure may occur. Monitor vital signs. Obtain a baseline ECG and institute continuous cardiac monitoring in patients with tachycardia. Sinus tachycardia does not generally require treatment unless hemodynamic compromise is present. If therapy is required, a short-acting, cardioselective agent such as esmolol is generally preferred.
Poisoning cause: MILD TO MODERATE Paroxetine TOXICITY
Toxic dose : 	>100 mg
Poisoning cause: SEVERE Paroxetine TOXICITY
Toxic dose : Per Olson guideline over	> 200–500 mg
Poisoning cause: MILD TO MODERATE Cymbalta (Duloxetine ) TOXICITY
Toxic dose : doses exceeding 120 mg daily, this but less than 1000 mg may lead to mild to moderate symptoms in adults. More than 7.4 mg/kg in children. 
Management: Most patients require only supportive care. Control agitation with either benzodiazepines. Serotonin syndrome generally responds to benzodiazepines, although a serotonin antagonist such as cyproheptadine may also be considered. Hypertension and tachycardia are generally mild and well tolerated, and do not require specific treatment.