SalioSAM/toxsample11 huggingface dataset:
Poisoning cause: SEVERE NISOLDIPINE TOXICITY
Toxic dose : Over 30 mg (adult), any (child)
Management: •Bradycardia and hypotension cases require standard ACLS care. •Consider central and arterial line placement. •Atropine may be used for bradycardia, but its effectiveness is limited in severe poisoning. •High-dose insulin and dextrose can be considered for hypotension refractory to other treatments. •Intravenous calcium (calcium chloride preferred) may have limited benefit in severe cases. •Standard vasopressors maintain blood pressure. •Lipid emulsion and glucagon are options for hypotension and variable success in severe cases. •Extracorporeal membrane oxygenation or cardiopulmonary bypass might be considered if standard treatments are ineffective. •Seizures can be treated with IV benzodiazepines, with potential use of barbiturates or propofol if needed.
Clinical effect 1: Profound bradycardia
Clinical effect 2: Dysrhythmia
Clinical effect 3: Complete heart block
Clinical effect 4: Hypotension
Clinical effect 5: Cardiogenic shock
Clinical effect 6: End-organ dysfunction
Clinical effect 7: Drowsiness/lethargy
Clinical effect 8: Syncope
Clinical effect 9: CNS depression
Clinical effect 10: Seizure
Clinical effect 11: Cerebral ischemia
Clinical effect 12: Bowel ischemia
Clinical effect 13: Renal failure
Clinical effect 14: Acidosis
Clinical effect 15: Coma
Clinical effect 16: Death
Clinical effect 17: Hyperglycemia
Poisoning cause: MILD TO MODERATE Diltiazem TOXICITY
Toxic dose : Over 120 mg (adult and Immediate-Release), 360 mg (adult and Sustained-Release), 540 mg (adult and Extended-Release), 1mg/kg (child)
Management: •Asymptomatic bradycardia patients should be observed with telemetry and peripheral IV access. •ECG monitoring and intravenous fluids can address mild hypotension
Clinical effect 1: Bradycardia
Clinical effect 2: Hypotension
Clinical effect 3: Dizziness
Clinical effect 4: Fatigue
Clinical effect 5: Lightheadedness
Poisoning cause: SEVERE Diltiazem TOXICITY
Toxic dose : Over 120 mg (adult and Immediate-Release), 360 mg (adult and Sustained-Release), 540 mg (adult and Extended-Release), 1mg/kg (child)
Management: •Bradycardia and hypotension cases require standard ACLS care. •Consider central and arterial line placement. •Atropine may be used for bradycardia, but its effectiveness is limited in severe poisoning. •High-dose insulin and dextrose can be considered for hypotension refractory to other treatments. •Intravenous calcium (calcium chloride preferred) may have limited benefit in severe cases. •Standard vasopressors maintain blood pressure. •Lipid emulsion and glucagon are options for hypotension and variable success in severe cases. •Extracorporeal membrane oxygenation or cardiopulmonary bypass might be considered if standard treatments are ineffective. •Seizures can be treated with IV benzodiazepines, with potential use of barbiturates or propofol if needed.
Clinical effect 1: Profound bradycardia
Clinical effect 2: Dysrhythmia
Clinical effect 3: Complete heart block
Clinical effect 4: Hypotension
Clinical effect 5: Cardiogenic shock
Clinical effect 6: End-organ dysfunction
Clinical effect 7: Drowsiness/lethargy
Clinical effect 8: Syncope
Clinical effect 9: CNS depression
Clinical effect 10: Seizure
Clinical effect 11: Cerebral ischemia
Clinical effect 12: Bowel ischemia
Clinical effect 13: Renal failure
Clinical effect 14: Acidosis
Clinical effect 15: Coma
Clinical effect 16: Death
Clinical effect 17: Hyperglycemia
Poisoning cause: MILD TO MODERATE Verapamil TOXICITY
Toxic dose : Over 120 mg (adult and Immediate-Release), 480 mg (adult and Sustained-Release), 2.5 mg/kg (child)
Management: •Asymptomatic bradycardia patients should be observed with telemetry and peripheral IV access. •ECG monitoring and intravenous fluids can address mild hypotension
Clinical effect 1: Bradycardia
Clinical effect 2: Hypotension
Clinical effect 3: Dizziness
Clinical effect 4: Fatigue
Clinical effect 5: Lightheadedness
Poisoning cause: SEVERE Verapamil TOXICITY
Toxic dose : Over 120 mg (adult and Immediate-Release), 480 mg (adult and Sustained-Release), 2.5 mg/kg (child)
Management: •Bradycardia and hypotension cases require standard ACLS care. •Consider central and arterial line placement. •Atropine may be used for bradycardia, but its effectiveness is limited in severe poisoning. •High-dose insulin and dextrose can be considered for hypotension refractory to other treatments. •Intravenous calcium (calcium chloride preferred) may have limited benefit in severe cases. •Standard vasopressors maintain blood pressure. •Lipid emulsion and glucagon are options for hypotension and variable success in severe cases. •Extracorporeal membrane oxygenation or cardiopulmonary bypass might be considered if standard treatments are ineffective. •Seizures can be treated with IV benzodiazepines, with potential use of barbiturates or propofol if needed.
Clinical effect 1: Profound bradycardia
Clinical effect 2: Dysrhythmia
Clinical effect 3: Complete heart block
Clinical effect 4: Hypotension
Clinical effect 5: Cardiogenic shock
Clinical effect 6: End-organ dysfunction
Clinical effect 7: Drowsiness/lethargy
Clinical effect 8: Syncope
Clinical effect 9: CNS depression
Clinical effect 10: Seizure
Clinical effect 11: Cerebral ischemia
Clinical effect 12: Bowel ischemia
Clinical effect 13: Renal failure
Clinical effect 14: Acidosis
Clinical effect 15: Coma
Clinical effect 16: Death
Clinical effect 17: Hyperglycemia
Poisoning cause: MILD TO MODERATE Nifedipine TOXICITY
Toxic dose : Over 30 mg (adult and Immediate-Release), 120 mg (adult and Extended-Release), any (child)
Management: Patients may have asymptomatic bradycardia or mild hypotension which may manifest as dizziness, fatigue, and/or lightheadedness
Clinical effect 1: Bradycardia
Clinical effect 2: Hypotension
Clinical effect 3: Dizziness
Clinical effect 4: Fatigue
Clinical effect 5: Lightheadedness
Poisoning cause: SEVERE Nifedipine TOXICITY
Toxic dose : Over 30 mg (adult and Immediate-Release), 120 mg (adult and Extended-Release), any (child)
Management: Can have profound bradycardia and dysrhythmias (including complete heart block) and hypotension resulting in cardiogenic shock and end-organ dysfunction including lethargy, syncope, altered mental status, seizures, cerebral ischemia, bowel ischemia, renal failure, metabolic acidosis, coma, and death. Hyperglycemia generally develops in patients with severe poisoning
Clinical effect 1: Profound bradycardia
Clinical effect 2: Dysrhythmia
Clinical effect 3: Complete heart block
Clinical effect 4: Hypotension
Clinical effect 5: Cardiogenic shock
Clinical effect 6: End-organ dysfunction
Clinical effect 7: Drowsiness/lethargy
Clinical effect 8: Syncope
Clinical effect 9: CNS depression
Clinical effect 10: Seizure
Clinical effect 11: Cerebral ischemia
Clinical effect 12: Bowel ischemia
Clinical effect 13: Renal failure
Clinical effect 14: Acidosis
Clinical effect 15: Coma
Clinical effect 16: Death
Clinical effect 17: Hyperglycemia
Poisoning cause: MILD TO MODERATE AMLODIPINE TOXICITY
Toxic dose : ADULT: Greater than 10 mg; CHILD: Greater than 0.3 mg/kg
Management: Patients who have asymptomatic bradycardia can be admitted and observed with telemetry. Obtain peripheral intravenous access and an ECG. Mild hypotension may only require treatment with intravenous fluid administration. 
Clinical effect 1: Reflex tachycardia
Clinical effect 2: Hypotension
Clinical effect 3: Drowsiness/lethargy
Clinical effect 4: Nausea
Clinical effect 5: Vomiting
Clinical effect 6: Peripheral vasodilation
Poisoning cause: SEVERE AMLODIPINE TOXICITY
Toxic dose : ADULT: Greater than 10 mg; CHILD: Greater than 0.3 mg/kg
Management: Patients with bradycardia and hypotension require standard ACLS treatment. Place a central line and consider placement of an arterial line. Standard first line treatment includes atropine for bradycardia although in a serious poisoning it is rarely effective. High dose insulin and dextrose have been effective in animal studies and multiple case reports in patients with hypotension refractory to other modalities, and should be considered early in patients with significant hypotension. Use intravenous calcium in severe poisonings although in these cases, beneficial effects of calcium infusion (calcium chloride is preferred) may be very minimal or short-lived. Repeat bolus doses or a continuous intravenous infusion are often needed. Standard vasopressors should be administered to maintain blood pressure. Lipid emulsion has been successful in animal studies and several case reports of patients with hypotension refractory to other therapies. Intravenous glucagon has been used with variable success. In a patient whose hemodynamic status continues to be refractory despite the treatment described above, extracorporeal membrane oxygenation or cardiopulmonary bypass should be considered. Treat seizures with IV benzodiazepines; barbiturates or propofol may be needed if seizures persist or recur.
Clinical effect 1: Profound hypotension
Clinical effect 2: Conduction disturbances/AV block
Clinical effect 3: Dysrhythmia
Clinical effect 4: Shock
Clinical effect 5: Acidosis
Clinical effect 6: Renal failure
Clinical effect 7: Respiratory depression
Clinical effect 8: Hypoxemia
Poisoning cause: MILD TO MODERATE Caffeine TOXICITY
Toxic dose : Over 30 mg/kg
Management: The earliest symptoms of acute caffeine poisoning include: anorexia, tremor, and restlessness, followed by nausea, vomiting and tachycardia. Chronic high-dose caffeine intake can lead to "caffeinism" which includes nervousness, twitching, anxiety, tremulousness, insomnia, palpitations, and hyperreflexia.
Clinical effect 1: Anorexia
Clinical effect 2: Tremor
Clinical effect 3: Agitation/Irritability/Restlessness
Clinical effect 4: Nausea
Clinical effect 5: Vomiting
Clinical effect 6: Tachycardia
Clinical effect 7: Nervousness
Clinical effect 8: Twitching
Clinical effect 9: Anxiety
Clinical effect 10: Tremulousness
Clinical effect 11: Insomnia
Clinical effect 12: Palpitations
Clinical effect 13: Hyperreflexia
Poisoning cause: SEVERE Caffeine TOXICITY
Toxic dose : Over 30 mg/kg
Management: With serious ingestions hypokalemia, hyperglycemia, metabolic acidosis, rhabdomyolysis, hypotension, confusion, seizures, tachycardia, and nonfatal dysrhythmias may occur.
Clinical effect 1: Hypokalemia
Clinical effect 2: Hyperglycemia
Clinical effect 3: Acidosis
Clinical effect 4: Rhabdomyolysis
Clinical effect 5: Hypotension
Clinical effect 6: Confusion
Clinical effect 7: Seizure
Clinical effect 8: Tachycardia
Clinical effect 9: Nonfatal dysrhythmia
Poisoning cause: MILD TO MODERATE Clonidine TOXICITY
Toxic dose : Over 0.1 mg (child under 4 years old), 0.2 mg (child from 5 to 8 years old), 0.4 mg (child Over 8 years old)
Management: There is no specific treatment. Hypotension should be treated with intravenous boluses of crystalloid. Bradycardia is typically mild and usually doesn't require any treatment. Bradycardia, hypotension and CNS depression often respond to physical stimulation. Naloxone has been used to reverse CNS depression with inconsistent success
Clinical effect 1: CNS depression
Clinical effect 2: Miosis
Clinical effect 3: Conduction disturbances/AV block
Clinical effect 4: Hypertension
Poisoning cause: SEVERE Clonidine TOXICITY
Toxic dose : Over 0.1 mg (child under 4 years old), 0.2 mg (child from 5 to 8 years old), 0.4 mg (child Over 8 years old)
Management: Severe bradycardia associated with hypotension and not responsive to physical stimulation should be treated with standard dose of atropine or cardiac pacing. Norepinephrine or dopamine may be beneficial in patients with severe bradycardia and hypotension not responding to physical stimulation, naloxone, intravenous crystalloid, and atropine. Patients with significant CNS and/or respiratory depression should be intubated. 
Clinical effect 1: Respiratory arrest
Clinical effect 2: Respiratory depression
Clinical effect 3: Coma
Clinical effect 4: Bradycardia
Clinical effect 5: Hypothermia
Clinical effect 6: Hypotension
Clinical effect 7: Early transient hypertension
Poisoning cause: Mild to Moderate AMITRIPTYLINE Toxicity
Toxic dose : Over 5 mg/kg (child), 300 mg (dose for adult), 200 mg (adolescent or elderly)
Management: •Isolated exposures can lead to a spectrum of toxicity, progressing from mild to severe. •For mild to moderate effects, consider activated charcoal within 2 hours of ingestion. •Aggressive care includes behavioral and temperature control, airway protection, blood pressure support, QRS monitoring and correction, and seizure management
Clinical effect 1: Drowsiness/lethargy
Clinical effect 2: Tachycardia
Clinical effect 3: Hallucinations
Clinical effect 4: Anticholinergic symptoms
Poisoning cause: Severe AMITRIPTYLINE Toxicity
Toxic dose : Over 5 mg/kg (child), 300 mg (dose for adult), 200 mg (adolescent or elderly).Based on Olson guidline>750–2000 mg
Management: •Activated charcoal remains relevant if within 2 hours of ingestion (airway protection first). •Aggressive care remains crucial, involving behavioral and temperature control, airway protection, blood pressure support, QRS monitoring and correction, and seizure management. •Intravenous lipid therapy is a consideration for ventricular dysrhythmias or hypotension
Clinical effect 1: Coma
Clinical effect 2: Seizure
Clinical effect 3: Dysrhythmia
Clinical effect 4: Respiratory depression
Clinical effect 5: Hypotension
Clinical effect 6: Delayed GI motility
Poisoning cause: Mild to Moderate CLOMIPRAMINE Toxicity
Toxic dose : Over 5 mg/kg (child), 300 mg (adult), 200 mg (from 10 to 18 years old)
Management: •Isolated exposures can lead to a spectrum of toxicity, progressing from mild to severe. •For mild to moderate effects, consider activated charcoal within 2 hours of ingestion. •Aggressive care includes behavioral and temperature control, airway protection, blood pressure support, QRS monitoring and correction, and seizure management.
Clinical effect 1: Drowsiness/lethargy
Clinical effect 2: Tachycardia
Clinical effect 3: Hallucinations
Clinical effect 4: Anticholinergic symptoms
Poisoning cause: Severe CLOMIPRAMINE Toxicity
Toxic dose : Over 5 mg/kg (child), 300 mg (adult), 200 mg (from 10 to 18 years old)
Management: •Activated charcoal remains relevant if within 2 hours of ingestion (airway protection first). •Aggressive care remains crucial, involving behavioral and temperature control, airway protection, blood pressure support, QRS monitoring and correction, and seizure management. •Intravenous lipid therapy is a consideration for ventricular dysrhythmias or hypotension.
Clinical effect 1: Coma
Clinical effect 2: Seizure
Clinical effect 3: Dysrhythmia
Clinical effect 4: Respiratory depression
Clinical effect 5: Hypotension
Clinical effect 6: Delayed GI motility
Poisoning cause: Mild to Moderate DESIPEAMINE Toxicity
Toxic dose : Over 2.5 mg/kg (child), 300 mg (dose for adult), 150 mg (adolescent or elderly)
Management: •Isolated exposures can lead to a spectrum of toxicity, progressing from mild to severe. •For mild to moderate effects, consider activated charcoal within 2 hours of ingestion. •Aggressive care includes behavioral and temperature control, airway protection, blood pressure support, QRS monitoring and correction, and seizure management.
Clinical effect 1: Drowsiness/lethargy
Clinical effect 2: Tachycardia
Clinical effect 3: Hallucinations
Clinical effect 4: Anticholinergic symptoms
Poisoning cause: Severe DESIPEAMINE E Toxicity
Toxic dose : Over 2.5 mg/kg (child), 300 mg (dose for adult), 150 mg (adolescent or elderly)
Management: •Activated charcoal remains relevant if within 2 hours of ingestion (airway protection first). •Aggressive care remains crucial, involving behavioral and temperature control, airway protection, blood pressure support, QRS monitoring and correction, and seizure management. •Intravenous lipid therapy is a consideration for ventricular dysrhythmias or hypotension
Clinical effect 1: Coma
Clinical effect 2: Seizure
Clinical effect 3: Dysrhythmia
Clinical effect 4: Respiratory depression
Clinical effect 5: Hypotension
Clinical effect 6: Delayed GI motility
Poisoning cause: Mild to Moderate DOXEPIN Toxicity
Toxic dose : Over 5 mg/kg (child), 300 mg (adult)
Management: •Toxicity ranges across a spectrum, with mild to moderate presentations possibly escalating to severe Over time. •For mild to moderate effects, activated charcoal is indicated if within 2 hours of ingestion. •Aggressive care involves behavioral and temperature control, safeguarding the airway, maintaining blood pressure, monitoring and correcting QRS interval, and managing seizures.
Clinical effect 1: Drowsiness/lethargy
Clinical effect 2: Tachycardia
Clinical effect 3: Hallucinations
Clinical effect 4: Anticholinergic symptoms
Poisoning cause: Severe DOXEPIN Toxicity
Toxic dose : Over 5 mg/kg (child), 300 mg (adult)
Management: •Activated charcoal is relevant within 2 hours of ingestion (prioritize airway protection). •Aggressive care remains imperative, including behavioral and temperature control, securing the airway, providing blood pressure support, monitoring and adjusting QRS interval, and managing seizures. •Intravenous lipid therapy is an early consideration for patients with ventricular dysrhythmias or hypotension.
Clinical effect 1: Coma
Clinical effect 2: Seizure
Clinical effect 3: Dysrhythmia
Clinical effect 4: Respiratory depression
Clinical effect 5: Hypotension
Clinical effect 6: Delayed GI motility
Poisoning cause: Mild to Moderate IMIPRAMINE Toxicity
Toxic dose : Over 5 mg/kg (child), 300 mg (dose for adult), 100 mg (adolescent or elderly)
Management: •Toxicity ranges across a spectrum, with mild to moderate presentations possibly escalating to severe Over time. •For mild to moderate effects, activated charcoal is indicated if within 2 hours of ingestion. •Aggressive care involves behavioral and temperature control, safeguarding the airway, maintaining blood pressure, monitoring and correcting QRS interval, and managing seizures
Clinical effect 1: Drowsiness/lethargy
Clinical effect 2: Tachycardia
Clinical effect 3: Hallucinations
Clinical effect 4: Anticholinergic symptoms
Poisoning cause: Severe IMIPRAMINE Toxicity
Toxic dose : Over 5 mg/kg (child), 300 mg (dose for adult), 100 mg (adolescent or elderly)
Management: •Activated charcoal is relevant within 2 hours of ingestion (prioritize airway protection). •Aggressive care remains imperative, including behavioral and temperature control, securing the airway, providing blood pressure support, monitoring and adjusting QRS interval, and managing seizures. •Intravenous lipid therapy is an early consideration for patients with ventricular dysrhythmias or hypotension
Clinical effect 1: Coma
Clinical effect 2: Seizure
Clinical effect 3: Dysrhythmia
Clinical effect 4: Respiratory depression
Clinical effect 5: Hypotension
Clinical effect 6: Delayed GI motility
Poisoning cause: Mild to Moderate NORTRIPTYLINE Toxicity
Toxic dose : Over 2.5 mg/kg (child), 150 mg (dose for adult), 50 mg (adolescent or elderly)
Management: •Toxicity ranges across a spectrum, with mild to moderate presentations possibly escalating to severe Over time. •For mild to moderate effects, activated charcoal is indicated if within 2 hours of ingestion. •Aggressive care involves behavioral and temperature control, safeguarding the airway, maintaining blood pressure, monitoring and correcting QRS interval, and managing seizures
Clinical effect 1: Drowsiness/lethargy
Clinical effect 2: Tachycardia
Clinical effect 3: Hallucinations
Clinical effect 4: Anticholinergic symptoms
Poisoning cause: Severe NORTRIPTYLINE Toxicity
Toxic dose : Over 2.5 mg/kg (child), 150 mg (dose for adult), 50 mg (adolescent or elderly)
Management: •Activated charcoal is relevant within 2 hours of ingestion (prioritize airway protection). •Aggressive care remains imperative, including behavioral and temperature control, securing the airway, providing blood pressure support, monitoring and adjusting QRS interval, and managing seizures. •Intravenous lipid therapy is an early consideration for patients with ventricular dysrhythmias or hypotension.
Clinical effect 1: Coma
Clinical effect 2: Seizure
Clinical effect 3: Dysrhythmia
Clinical effect 4: Respiratory depression
Clinical effect 5: Hypotension
Clinical effect 6: Delayed GI motility
Poisoning cause: Mild to Moderate PROTRIPTYLINE Toxicity
Toxic dose : Over 1 mg/kg (child), 60 mg (dose for adult), 20 mg (adolescent or elderly)
Management: Lower doses lead to symptoms like drowsiness, sedation, tachycardia, hallucinations, and anticholinergic effects.
Clinical effect 1: Drowsiness/lethargy
Clinical effect 2: Tachycardia
Clinical effect 3: Hallucinations
Clinical effect 4: Anticholinergic symptoms
Poisoning cause: Severe PROTRIPTYLINE Toxicity
Toxic dose : Over 1 mg/kg (child), 60 mg (dose for adult), 20 mg (adolescent or elderly)
Management: •Activated charcoal is relevant within 2 hours of ingestion (prioritize airway protection). •Aggressive care remains imperative, including behavioral and temperature control, securing the airway, providing blood pressure support, monitoring and adjusting QRS interval, and managing seizures. •Intravenous lipid therapy is an early consideration for patients with ventricular dysrhythmias or hypotension.
Clinical effect 1: Coma
Clinical effect 2: Seizure
Clinical effect 3: Dysrhythmia
Clinical effect 4: Respiratory depression
Clinical effect 5: Hypotension
Clinical effect 6: Delayed GI motility
Poisoning cause: Mild to Moderate TRIMIPRAMINE Toxicity
Toxic dose : Over 2.5 mg/kg (child), 200 mg (adult), 100 mg (adolescent or elderly)
Management: •Toxicity ranges across a spectrum, with mild to moderate presentations possibly escalating to severe Over time. •For mild to moderate effects, activated charcoal is indicated if within 2 hours of ingestion. •Aggressive care involves behavioral and temperature control, safeguarding the airway, maintaining blood pressure, monitoring and correcting QRS interval, and managing seizures.
Clinical effect 1: Drowsiness/lethargy
Clinical effect 2: Tachycardia
Clinical effect 3: Hallucinations
Clinical effect 4: Anticholinergic symptoms
Poisoning cause: Severe TRIMIPRAMINE Toxicity
Toxic dose : Over 2.5 mg/kg (child), 200 mg (adult), 100 mg (adolescent or elderly)
Management: •Activated charcoal is relevant within 2 hours of ingestion (prioritize airway protection). •Aggressive care remains imperative, including behavioral and temperature control, securing the airway, providing blood pressure support, monitoring and adjusting QRS interval, and managing seizures. •Intravenous lipid therapy is an early consideration for patients with ventricular dysrhythmias or hypotension.
Clinical effect 1: Coma
Clinical effect 2: Seizure
Clinical effect 3: Dysrhythmia
Clinical effect 4: Respiratory depression
Clinical effect 5: Hypotension
Clinical effect 6: Delayed GI motility
Poisoning cause: MILD TO MODERATE Duloxetine (Cymbalta) TOXICITY
Toxic dose : 6 months - 6 years	>60 mg,
7 years - 17 years	>180 mg,
18 years - 79 years	>300 mg
Management: •Supportive care is the mainstay. •Agitation can be managed with benzodiazepines. •Serotonin syndrome can be addressed with benzodiazepines or cyproheptadine. •Mild hypertension and tachycardia often don't need specific treatment.
Clinical effect 1: Drowsiness/lethargy
Clinical effect 2: Syncope
Clinical effect 3: Tachycardia
Clinical effect 4: Vomiting
Clinical effect 5: Diarrhea
Clinical effect 6: Headaches
Clinical effect 7: Diaphoresis
Clinical effect 8: Agitation/Irritability/Restlessness
Clinical effect 9: Confusion
Clinical effect 10: Hypertension