SalioSAM/toxsample11 huggingface dataset:
Poisoning cause: Mild to Moderate Venlafaxine or desvenlafaxine Toxicity
Toxic dose : Toxic dose of Venlafaxine in a Child: An inadvertent ingestion of Venlafaxine > 5.5 mg/kg venlafaxine The patient should go to the ER if >10 mg/kg or more than 1000 mg.In adults, toxic effects might be observed with doses exceeding approximately 937.5 mg.  Per Olson guideline over 300-6000 mg
Management: Supportive care is the primary approach for mild/moderate toxicity. Benzodiazepines are preferred for treating agitation, mild serotonergic effects, and hyperadrenergic signs. Intravenous fluids are used for mild hypotension. Viloxazine use can lead to increased diastolic blood pressure.
Clinical effect 1: Tremor
Clinical effect 2: Hyperreflexia
Clinical effect 3: Anxiety
Clinical effect 4: Agitation/Irritability/Restlessness
Clinical effect 5: Palpitations
Clinical effect 6: Tachycardia
Clinical effect 7: Heart failure exacerbation
Clinical effect 8: Drowsiness/lethargy
Poisoning cause: Severe Venlafaxine or desvenlafaxine Toxicity
Toxic dose :  serious toxicity, including seizures, serotonin syndrome, and cardiac arrhythmias, has been reported with ingestions of greater than 1 gram (1000 mg):Doses larger than 1500 mg have been associated with seizures. Cardiovascular toxicity, manifested by dangerous arrhythmias, can occur with dosages larger than 8000 mg. Per Olson guideline over 300-6000 mg
Management: Benzodiazepines are employed for seizures and agitation, often requiring higher doses. Intubation and sedation with propofol or barbiturates are considered for unresponsive agitation, tachycardia, fever, or seizures. Neuromuscular paralysis with continuous EEG monitoring is an option if hyperthermia persists. Isotonic fluids are given to address insensible losses, clear myoglobin, and enhance renal clearance. Vasopressors might be needed for severe hypotension; insulin, dextrose, or intravenous fat emulsion therapy can be considered. Extracorporeal support may be necessary for unstable patients despite medical therapy
Clinical effect 1: Altered mental state
Clinical effect 2: Muscle rigidity
Clinical effect 3: Autonomic instability
Clinical effect 4: Prolonged PR
Clinical effect 5: QRS widening
Clinical effect 6: Prolonged qtc
Clinical effect 7: Seizure
Clinical effect 8: Rhabdomyolysis
Clinical effect 9: Eosinophilic pneumonia
Clinical effect 10: Coma
Clinical effect 11: Delirium
Poisoning cause: Mild to Moderate Zolpidem Toxicity
Toxic dose : Over 70 mg (adult), 2.5 mg (child)
Management: Supportive care
Clinical effect 1: Drowsiness/lethargy
Clinical effect 2: Slurred speech
Clinical effect 3: Confusion
Clinical effect 4: Ataxia
Poisoning cause: Severe Zolpidem Toxicity
Toxic dose : Over 70 mg (adult), 2.5 mg (child)
Management: •Severe toxicity is more likely when other sedating substances are ingested concurrently. •Administer activated charcoal if the ingestion is recent and the patient is alert or the airway is protected. •Consider orotracheal intubation for airway protection if the patient becomes increasingly drowsy or comatose
Clinical effect 1: Hypotension
Clinical effect 2: Coma
Clinical effect 3: Respiratory depression
Poisoning cause: Mild to moderate warfarin toxicity
Toxic dose : Over 0.5 mg/kg (child), adults:over >1 mg/kg OR >50 mg
Toxic serum or urine levels: INR: >1.5 but <3.0
Management: Monitor INR and hemoglobin levels, and assess for any clinical signs of bleeding. Consider withholding warfarin until INR approaches the therapeutic range.
Clinical effect 1: Bleeding
Clinical effect 2: Epistaxis
Clinical effect 3: Bleeding from gums
Clinical effect 4: Ecchymosis
Clinical effect 5: Hematochezia
Clinical effect 6: Hematuria
Clinical effect 7: Menorrhagia
Clinical effect 8: Hemarthrosis
Clinical effect 9: Bleeding from minor skin or soft tissue trauma
Poisoning cause: SEVERE Warfarin TOXICITY
Toxic dose : Over 0.5 mg/kg (child), adults:over 	>1 mg/kg OR >50 mg
Toxic serum or urine levels: Moderate Warfarin Toxicity:INR: 3.0 to 4.5.Severe Warfarin Toxicity: INR: >4.5. Life-threatening Warfarin Toxicity:INR: Significantly elevated, often >10
Management: 1.Provide supportive care, including administration of intravenous crystalloids, oxygen, and mechanical ventilation if necessary. 2 In cases of significant bleeding, hemorrhagic shock may occur, requiring transfusions of packed red blood cells and fresh frozen plasma. Factor concentrates like cryoprecipitate or 4-factor prothrombin complex concentrate (PCC) may be needed for severe bleeding. 3.Administer Vitamin K1; larger doses might be necessary for substantial ingestions. 4. Surgical consultation may be necessary based on the extent and location of hemorrhage.
Clinical effect 1: Intracranial hemorrhage
Clinical effect 2: Retroperitoneal hemorrhage
Clinical effect 3: Massive gastrointestinal bleed
Poisoning cause: MILD TO MODERATE Oil of wintergreen TOXICITY
Toxic dose : Over 1 mg (child under 6 years old), 4 cc (child Over 6 years old).The acute ingestion of less than 150 mg/kg or 6.5 g of aspirin equivalent, whichever is less, is not expected to cause significant toxicity. For oil of wintergreen (98% methyl salicylate), greater than a lick or taste by children under 6 years of age or greater than 4 mL by patients 6 years of age and older may cause toxicity and requires referral to an emergency department for evaluation.
Management: An initial salicylate level should be obtained and repeated every 1 to 2 hours until a clear peak and decline in concentration is observed. Concentrations greater than 30 mg/dL and rising should be treated with urine alkalinization. The presence of a large anion gap metabolic acidosis or altered mental status indicates a more severe poisoning.
Clinical effect 1: Abdominal pain
Clinical effect 2: Tinnitus
Clinical effect 3: Hyperventilation/tachypnea
Clinical effect 4: Respiratory alkalosis
Poisoning cause: Severe Acute Oil of wintergreen TOXICITY
Toxic dose : Over 1 mg (child under 6 years old), 4 cc (child Over 6 years old).The acute ingestion of less than 150 mg/kg or 6.5 g of aspirin equivalent, whichever is less, is not expected to cause significant toxicity. For oil of wintergreen (98% methyl salicylate), greater than a lick or taste by children under 6 years of age or greater than 4 mL by patients 6 years of age and older may cause toxicity and requires referral to an emergency department for evaluation.
B) FATALITIES: As little as 5 mL of oil of wintergreen has resulted in pediatric deaths.
Management: Patients with severe poisoning should be continued on urine alkalinization. Hemodialysis should be strongly considered. Relative indications for hemodialysis include: renal failure, congestive heart failure, altered mental status, seizures, evidence of cerebral edema, worsening acidosis despite adequate resuscitation, persistently rising salicylate concentrations despite adequate treatment (greater than 50 to 60 mg/dL in a chronic poisoning or levels greater than 90 to 100 mg/dL in an acute Overdose). Patients with an altered mental status may have cerebral edema. Obtain a head CT. Mannitol can be given for cerebral edema. Severely ill patients may require respiratory support and intubation. Maintain preintubation minute ventilation at the same high respiratory rate because once the patient's respiratory drive is removed metabolic acidosis may worsen. 
Clinical effect 1: Acidosis
Clinical effect 2: Hyperpnea
Clinical effect 3: Diaphoresis
Clinical effect 4: Fever/hyperthermia
Clinical effect 5: CNS depression
Clinical effect 6: Seizure
Clinical effect 7: Coma
Clinical effect 8: Cerebral edema
Clinical effect 9: Pulmonary edema
Clinical effect 10: Death
Poisoning cause: Severe Chronic Oil of wintergreen TOXICITY
Toxic dose : Over 1 mg (child under 6 years old), 4 cc (child Over 6 years old).Ingestions of greater than 100 mg/kg/day Over 2 days may produce toxicity. 
Management: Patients with severe poisoning should be continued on urine alkalinization. Hemodialysis should be strongly considered. Relative indications for hemodialysis include: renal failure, congestive heart failure, altered mental status, seizures, evidence of cerebral edema, worsening acidosis despite adequate resuscitation, persistently rising salicylate concentrations despite adequate treatment (greater than 50 to 60 mg/dL in a chronic poisoning or levels greater than 90 to 100 mg/dL in an acute Overdose). Patients with an altered mental status may have cerebral edema. Obtain a head CT. Mannitol can be given for cerebral edema. Severely ill patients may require respiratory support and intubation. Maintain preintubation minute ventilation at the same high respiratory rate because once the patient's respiratory drive is removed metabolic acidosis may worsen. 
Clinical effect 6: Other LFTs abnormality
Clinical effect 7: Dysrhythmia
Poisoning cause: MILD TO MODERATE Bromadiolone and other Long-acting Anticoagulant Rodenticide TOXICITY
Toxic dose : Over 1 mg
Management: Most unintentional ingestions (e.g., in children under 6) may not require treatment. Monitor asymptomatic INR elevation and consider vitamin K if INR is significantly prolonged (>2.0).
Clinical effect 1: Asymptomatic
Clinical effect 2: Minimal bleeding
Clinical effect 3: Easy bruising
Poisoning cause: SEVERE Bromadiolone and other Long-acting Anticoagulant Rodenticide TOXICITY
Toxic dose : Over 1 mg
Management: Life-threatening bleeding requires rapid coagulopathy reversal with FFP or prothrombin complex concentrate. Administer vitamin K intravenously or subcutaneously initially, then orally once stable. Long-term vitamin K use may be needed (weeks to months).
Clinical effect 1: Severe bleeding diathesis
Clinical effect 2: GI bleeding
Clinical effect 3: Intracranial bleeding
Clinical effect 4: Hematuria
Clinical effect 5: Intraabdominal bleeding
Clinical effect 6: Retroperitoneal bleeding
Poisoning cause: Mild to Moderate Iron Toxicity
Toxic dose : Over 20 mg/kg (potentially toxic), Over 40 mg/kg (toxic)
Management: Supportive care with IV fluids; activated charcoal not effective for iron ingestions. Symptomatic patients need observation for deterioration and acidosis. Abdominal x-rays (radiopaque tablets) and iron concentration measurement recommended. Consider whole bowel irrigation for large tablet ingestion. Iron concentration checked 4-6 hours post-ingestion, repeated in 2-4 hours. Chelation for metabolic acidosis or worsening despite IV hydration
Clinical effect 1: Vomiting
Clinical effect 2: Diarrhea
Poisoning cause: Severe Iron Toxicity
Toxic dose : Over 20 mg/kg (potentially toxic), Over 40 mg/kg (toxic)
Management: Deferoxamine chelation for severe poisoning signs (shock, acidosis, GI bleeding, lethargy/coma). Consider chelation if serum iron >500 mcg/dL, especially with significant symptoms. Blood transfusions if significant GI bleeding
Clinical effect 1: Severe vomiting
Clinical effect 2: Diarrhea
Clinical effect 3: Drowsiness/lethargy
Clinical effect 4: Acidosis
Clinical effect 5: Shock
Clinical effect 6: GI bleeding
Clinical effect 7: Coma
Clinical effect 8: Seizure
Clinical effect 9: Mild Elevation of serum transaminase (Alt,Ast<100)
Clinical effect 11: Bilirubin increased
Clinical effect 12: Other LFTs abnormality
Clinical effect 13: Late onset GI strictures
Clinical effect 14: Cyanosis
Clinical effect 15: Fever/hyperthermia
Clinical effect 16: Decreased plasma volume
Clinical effect 17: Hypotension
Clinical effect 18: CNS depression
Clinical effect 19: Acute lung injury
Poisoning cause: Mild to Moderate Boric Acid (Borate) Toxicity
Toxic dose : Over 1000 mg (infant), 2000 mg (child), 7000 mg (adult)
Management: Supportive care with hydration, antiemetics, and electrolyte repletion usually sufficient
Clinical effect 1: Nausea
Clinical effect 2: Vomiting
Clinical effect 3: Diarrhea
Clinical effect 4: Skin erythema
Clinical effect 5: Skin peeling
Poisoning cause: Severe Boric Acid (Borate) Toxicity
Toxic dose : Over 1000 mg (infant), 2000 mg (child), 7000 mg (adult)
Management: Supportive care, consider dialysis. For hypotension, infuse isotonic fluid; if persistent, administer dopamine or norepinephrine. Benzodiazepines for seizures; phenobarbital or propofol if needed. Monitor serum creatine phosphokinase and creatinine; watch for rhabdomyolysis
Clinical effect 1: Dehydration
Clinical effect 2: Hypotension
Clinical effect 3: Hallucinations/delusions
Clinical effect 4: Agitation/irritablity
Clinical effect 5: CNS depression
Clinical effect 6: Drowsiness/lethargy
Clinical effect 7: Seizure
Clinical effect 8: Coma
Clinical effect 9: Renal failure
Clinical effect 10: Dysrhythmia
Clinical effect 11: Acidosis
Clinical effect 12: Rhabdomyolysis
Clinical effect 13: Corrosive injury
Clinical effect 14: Esophageal ulceration
Clinical effect 15: Gastric ulceration
Poisoning cause: Mild to Moderate Bupropion (Wellbutrin) Toxicity
Toxic dose : Over 600 mg (adult and Immediate-Release), 900 mg (adult and Sustained-Release), 10 mg/kg (child)
Management: Most buPROPion Overdoses require only supportive care. Treat agitation, tremors, or seizures with benzodiazepines. Hypertension and tachycardia are generally mild and well tolerated, and do not require specific treatment
Clinical effect 1: Tachycardia
Clinical effect 2: Hypertension
Clinical effect 3: Single self-limited seizure
Clinical effect 4: Agitation/Irritability/Restlessness
Clinical effect 5: Dizziness
Clinical effect 6: Tremor
Clinical effect 7: Paresthesia
Clinical effect 8: Slurred speech
Clinical effect 9: Drowsiness/lethargy
Clinical effect 10: Confusion
Clinical effect 11: Hallucinations
Clinical effect 12: Vomiting
Poisoning cause: Severe Bupropion (Wellbutrin) Toxicity
Toxic dose : Over 600 mg (adult and Immediate-Release), 900 mg (adult and Sustained-Release), 10 mg/kg (child).Per Olson guidline , seizures can occur in some patients with moderate overdose or even in therapeutic doses. Therefore, the range of toxicity might start as low as 2000 mg or even lower in sensitive individuals.
Management: Treat seizures with benzodiazepines; recurrent seizures may require the addition of barbiturates or propofol. Treat hypotension with fluids and pressors if needed, central venous pressure monitoring may help guide therapy of persistent hypotension. Treat ventricular dysrhythmias with intravenous sodium bicarbonate, or lidocaine if bicarbonate is unsuccessful. Consider intravenous lipid therapy early for patients with ventricular dysrhythmias or hypotension. Manage airway in patients with CNS depression or recurrent seizures. QTc prolongation rarely requires treatment
Clinical effect 1: Recurrent seizure
Clinical effect 2: Status epilepticus
Clinical effect 3: Hyperthermia
Clinical effect 4: Hypotension
Clinical effect 5: Coma
Clinical effect 6: QRS widening
Clinical effect 7: QTc prolongation
Clinical effect 8: Ventricular dysrhythmia
Poisoning cause: MILD TO MODERATE Camphor TOXICITY
Toxic dose : Over 10 mg/kg (mild to moderate), 30 mg/kg (serious)
Management: Supportive care with fluids and benzodiazepines will treat most toxic sequelae. Tachycardia is well-tolerated and no specific treatment, other than fluid resuscitation and benzodiazepines, is necessary
Clinical effect 1: Nausea
Clinical effect 2: Vomiting
Clinical effect 3: Seizure
Poisoning cause: SEVERE Camphor TOXICITY
Toxic dose : Over 10 mg/kg (mild to moderate), 30 mg/kg (serious)
Management: Airway management may be necessary for severe CNS depression or recalcitrant seizures. Status epilepticus should be treated with high-dose benzodiazepines followed by propofol or phenobarbital, if benzodiazepines are ineffective. Fluid resuscitation should be the first line treatment for hypotension. Hypotension unresponsive to fluids should be treated with vasopressors.
Clinical effect 1: Delirium
Clinical effect 2: Visual hallucinations
Clinical effect 3: Cerebral edema
Clinical effect 4: Status epilepticus
Clinical effect 5: Hypotension
Clinical effect 6: Tachycardia
Clinical effect 7: Respiratory depression
Poisoning cause: MILD TO MODERATE Bepridil (Bepadin) TOXICITY
Toxic dose : Over 300 mg (adult), any (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 Bepridil (Bepadin) TOXICITY
Toxic dose : Over 300 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 ISRADIPINE TOXICITY
Toxic dose : Over 20 mg (adult), 0.1 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 ISRADIPINE TOXICITY
Toxic dose : Over 20 mg (adult), 0.1 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 NICARDIPINE TOXICITY
Toxic dose : Over 40 mg (adult and Immediate-Release), 60 mg (adult and Sustained-Release), 1.25 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 NICARDIPINE TOXICITY
Toxic dose : Over 40 mg (adult and Immediate-Release), 60 mg (adult and Sustained-Release), 1.25 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 NIMODIPINE TOXICITY
Toxic dose : Over 60 mg (adult), 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 NIMODIPINE TOXICITY
Toxic dose : Over 60 mg (adult), 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 NISOLDIPINE TOXICITY
Toxic dose : Over 30 mg (adult), any (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