SalioSAM/toxsample11 huggingface dataset:
Poisoning cause: Severe Lead Toxicity
Toxic serum or urine levels: Over 40 mcg /dL, usually needs chelator treatment).Blood lead levels of 60–80 mcg/dL may cause gastrointestinal symptoms and subclinical renal effects, while levels above 80 mcg/dL can lead to serious overt intoxication, including abdominal pain and nephropathy. Encephalopathy and neuropathy usually occur with levels over 100 mcg/dL​​.
Management: Acute ingestions of very large amounts of lead are rare, but may cause abdominal pain, nausea, vomiting, anemia (usually hemolytic), toxic hepatitis, and encephalopathy. In children, severe toxicity manifests as encephalopathy (ie, coma, seizures, ataxia, incoordination, cranial nerve palsies, increased intracranial pressure, bizarre behavior or altered mentation), persistent vomiting, and anemia. More severe subacute or chronic exposures in adults can lead to symptoms such as fatigue, malaise, irritability, anorexia, insomnia, weight loss, decreased libido, arthralgias, myalgias, hypertension, crampy abdominal pain, nausea, constipation or diarrhea (less commonly), impaired concentration, headache, diminished visual-motor coordination, tremor, encephalopathy, a peripheral motor neuropathy (especially affecting the upper extremities causing wrist drops), a normochromatic or microcytic anemia (the hallmark of which is basophilic stippling), nephrotoxicity (a reversible acute tubular dysfunction and chronic interstitial fibrosis), hyperuricemia, and associated gout.
Clinical effect 1: Abdominal pain
Clinical effect 2: Nausea
Clinical effect 3: Vomiting
Clinical effect 4: Anemia
Clinical effect 5: Toxic hepatitis
Clinical effect 6: Delirium/encephalopathy
Clinical effect 7: Coma
Clinical effect 8: Seizure
Clinical effect 9: Ataxia
Clinical effect 10: Incoordination
Clinical effect 11: Cranial nerve palsies
Clinical effect 12: Increased intracranial pressure
Clinical effect 13: Behavioral changes/Bizarre behavior / altered mentation
Clinical effect 14: Intermittent/persistent vomiting
Clinical effect 15: Fatigue
Clinical effect 16: Malaise
Clinical effect 17: Agitation/Irritability/Restlessness
Clinical effect 18: Anorexia
Clinical effect 19: Insomnia
Clinical effect 20: Weight loss
Clinical effect 21: Decreased libido
Clinical effect 22: Arthralgias
Clinical effect 23: Myalgias
Clinical effect 24: Hypertension
Clinical effect 25: Crampy abdominal pain
Clinical effect 26: Constipation
Clinical effect 27: Diarrhea
Clinical effect 28: Impaired concentration
Clinical effect 29: Headache
Clinical effect 30: Diminished visual-motor coordination
Clinical effect 31: Tremor
Clinical effect 32: Peripheral motor neuropathy
Clinical effect 33: Wrist drops
Clinical effect 34: Normochromatic anemia
Clinical effect 35: Microcytic anemia basophilic stippling
Clinical effect 36: Nephrotoxicity
Clinical effect 37: Reversible acute tubular dysfunction
Clinical effect 38: Chronic interstitial fibrosis
Clinical effect 39: Hyperuricemia
Clinical effect 40: Associated gout
Poisoning cause: Mild to Moderate Acute Digoxin Toxicity
Toxic dose : Over 3 mg (adult and acute), Over 1 mg (children)
Toxic serum or urine levels:  10 ng/mL (acute)
Management: Patients who do not develop significant cardiac toxicity require only supportive care and monitoring. Patients with mild bradycardia and nonspecific symptoms from chronic poisoning should be monitored and rehydrated, but do not require specific therapy.
Clinical effect 1: Nausea
Clinical effect 2: Vomiting
Clinical effect 3: Abdominal pain
Clinical effect 4: Drowsiness/lethargy
Clinical effect 5: Bradycardia
Poisoning cause: Mild to Moderate Chronic Digoxin Toxicity
Toxic dose : Over 0.1 mg/kg (children)
Toxic serum or urine levels: Over 2 ng/mL (acute on chronic or chronic)
Management: Patients who do not develop significant cardiac toxicity require only supportive care and monitoring. Patients with mild bradycardia and nonspecific symptoms from chronic poisoning should be monitored and rehydrated, but do not require specific therapy.
Clinical effect 1: Bradycardia
Clinical effect 2: Malaise
Clinical effect 3: Nausea
Clinical effect 4: Anorexia
Clinical effect 5: Delirium
Clinical effect 6: Visual impairment
Poisoning cause: Severe Acute Digoxin Toxicity
Toxic dose : Over 3 mg (adult and acute), Over 1 mg (children).Serum potassium levels higher than 5.5 mEq/L suggest severe poisoning​​.
Toxic serum or urine levels:  10 ng/mL (acute)
Management: Following acute ingestion, patients with hyperkalemia (greater than 5 mEq/L), symptomatic bradycardia, ventricular ectopy, or dysrhythmias should be treated with digoxin immune Fab. Digoxin immune Fab is also indicated for patients with chronic toxicity with ventricular ectopy or symptomatic bradycardia. If digoxin immune Fab is not available, patients can be treated with atropine or cardiac pacing for bradycardia and antidysrhythmics (lidocaine or amiodarone) for ventricular ectopy or dysrhythmias. Other treatments have been suggested. Phenytoin (100 mg to 300 mg IV bolus) and magnesium sulfate (2 g) have both been anecdotally reported to produce resolution of dysrhythmias from cardiac glycoside poisoning. Finally, cardiac pacing (at a rate that exceeds cardiac ectopy) can be used for patients who do not respond to medical management.

Summary of Digoxin Immune Fab (Digoxin-Specific Antibody Fragments) for Cardiac Glycoside Poisoning:
Antidote: Digoxin immune Fab (digoxin immune antibody fragment)
Indications of Digoxin immune Fab:
Severe Toxicity: Ventricular dysrhythmias, progressive bradyarrhythmias, 2nd or 3rd degree heart block.
Refractory Hypotension: In cases of severe toxicity.
Hyperkalemia: If serum potassium level is greater than 5 mEq/L in acute Overdose.
Risk of Cardiac Arrest: Ingestion of digoxin greater than 10 mg in adults or greater than 4 mg in children, serum digoxin concentration greater than 10 ng/mL post-distribution (around 6 hours after ingestion).
Lack of Response to Conventional Therapy: When conventional treatments do not work effectively.
Dosage Calculation:
By Ingested Dose:
Digoxin immune Fab dose (in vials) = Ingested dose of capsules (in mg) / 0.5 mg per vial
Digoxin immune Fab dose (in vials) = Ingested dose of tablets (in mg) * 0.8 (for 80% bioavailability) / 0.5 mg per vial
By Steady State Concentration:
Digoxin immune Fab dose (in vials) = Steady state serum digoxin concentration (in ng/mL) * Patient weight (in kg) / 100
Administration: Administer 10 to 20 vials for critically ill patients or patients in cardiac arrest.

Clinical effect 1: Bradycardia
Clinical effect 2: Heart block
Clinical effect 3: Vomiting
Clinical effect 4: Shock
Clinical effect 5: Hyperkalemia
Poisoning cause: Severe Chronic Digoxin Toxicity
Toxic dose : Over 0.1 mg/kg (children)
Toxic serum or urine levels: Over 2 ng/mL (acute on chronic or chronic)
Management: Following acute ingestion, patients with hyperkalemia (greater than 5 mEq/L), symptomatic bradycardia, ventricular ectopy, or dysrhythmias should be treated with digoxin immune Fab. Digoxin immune Fab is also indicated for patients with chronic toxicity with ventricular ectopy or symptomatic bradycardia. If digoxin immune Fab is not available, patients can be treated with atropine or cardiac pacing for bradycardia and antidysrhythmics (lidocaine or amiodarone) for ventricular ectopy or dysrhythmias. Other treatments have been suggested. Phenytoin (100 mg to 300 mg IV bolus) and magnesium sulfate (2 g) have both been anecdotally reported to produce resolution of dysrhythmias from cardiac glycoside poisoning. Finally, cardiac pacing (at a rate that exceeds cardiac ectopy) can be used for patients who do not respond to medical management.

Summary of Digoxin Immune Fab (Digoxin-Specific Antibody Fragments) for Cardiac Glycoside Poisoning:
Antidote: Digoxin immune Fab (digoxin immune antibody fragment)
Indications of Digoxin immune Fab:
Severe Toxicity: Ventricular dysrhythmias, progressive bradyarrhythmias, 2nd or 3rd degree heart block.
Refractory Hypotension: In cases of severe toxicity.
Hyperkalemia: If serum potassium level is greater than 5 mEq/L in acute Overdose.
Risk of Cardiac Arrest: Ingestion of digoxin greater than 10 mg in adults or greater than 4 mg in children, serum digoxin concentration greater than 10 ng/mL post-distribution (around 6 hours after ingestion).
Lack of Response to Conventional Therapy: When conventional treatments do not work effectively.
Dosage Calculation:
By Ingested Dose:
Digoxin immune Fab dose (in vials) = Ingested dose of capsules (in mg) / 0.5 mg per vial
Digoxin immune Fab dose (in vials) = Ingested dose of tablets (in mg) * 0.8 (for 80% bioavailability) / 0.5 mg per vial
By Steady State Concentration:
Digoxin immune Fab dose (in vials) = Steady state serum digoxin concentration (in ng/mL) * Patient weight (in kg) / 100
Administration: Administer 10 to 20 vials for critically ill patients or patients in cardiac arrest.

Clinical effect 1: Ventricular dysrhythmia
Clinical effect 2: Conduction disturbances/AV block
Clinical effect 3: Hyperkalemia
Poisoning cause: Mild to Moderate Phenytoin Toxicity
Toxic dose : Over 20 mg/kg
Toxic serum or urine levels: Over 20 to 50 µg/mL (mild to moderate), Nystagmus is common at serum concentrations above 20 mg/L, ataxia, slurred speech, and tremor above 30 mg/L.
Management: For mild and moderate toxicity, treat with supportive care, as the patient eventually metabolizes the phenytoin. If the patient is awake and alert, administer a dose of activated charcoal. Protect the patient from self-injury secondary to ataxia.
Clinical effect 1: Nausea
Clinical effect 2: Vomiting
Clinical effect 3: Nystagmus
Clinical effect 4: Ataxia
Clinical effect 5: CNS depression
Poisoning cause: Severe Phenytoin Toxicity
Toxic dose : Over  20 mg/kg
Toxic serum or urine levels: Over 50 µg/mL (severe).lethargy, confusion, and stupor ensue with levels higher than 40 mg/L. 
Management: For large phenytoin Overdoses, treat with supportive care, which may include intubation for comatose patients. If seizures do occur, treat with benzodiazepines and evaluate for other causes of seizures.
Clinical effect 1: Coma
Clinical effect 3: Respiratory depression
Poisoning cause: Severe Methanol toxicity
Toxic dose : The minimum toxic dose of methanol is approximately 100 mg/kg​​
Toxic serum or urine levels: Over 40 mg/dL
Management:  Patients presenting with severe acidosis, signs or symptoms of visual changes, or depressed level of consciousness should be started immediately on an ADH inhibitor and intravenous folate. Hemodialysis should be initiated and should be continued until the methanol concentration is undetectable and the serum pH is normal. Treat seizures with benzodiazepines.
Clinical effect 1:  acidosis
Clinical effect 2: Multiorgan dysfunction
Clinical effect 3: Hypotension
Clinical effect 4: Tachycardia
Clinical effect 5: Dysrhythmias
Clinical effect 6: Seizures
Clinical effect 7: Coma
Clinical effect 8: Pancreatitis
Clinical effect 9: Acute renal failure
Clinical effect 10: Rhabdomyolysis
Clinical effect 11: Hypomagnesemia
Clinical effect 12: Hypokalemia
Clinical effect 13: Hypophosphatemia
Clinical effect 14: Mydriasis
Clinical effect 15: Hyperemic optic discs
Clinical effect 16: Papilledema
Clinical effect 17: Visual impairment
Clinical effect 18: Blindness
Clinical effect 19: Basal ganglia necrosis
Clinical effect 20: Parkinsonian features
Clinical effect 21: Tremor
Clinical effect 22: Rigidity
Clinical effect 23: Bradykinesia
Clinical effect 24: Blindness
Poisoning cause: Mild Methanol Toxicity
Toxic dose : The minimum toxic dose of methanol is approximately 100 mg/kg​​
Toxic serum or urine levels: Over 25 mg/dL
Management: Obtain a methanol level, serum chemistry, and a serum pH. A thorough visual exam should be performed, including visual acuity. An elevated osmolar gap suggests the presence of methanol or another alcohol but cannot be used to rule out a significant exposure. If a methanol concentration is readily available (results known within 2 hours) and the patient is asymptomatic, then alcohol dehydrogenase (ADH) inhibition can be delayed until the methanol concentration is available. Patients with a methanol concentration of more than 25 mg/dL or metabolic acidosis should be treated with ADH inhibition. If methanol concentrations cannot readily be measured, patients with a history of a potentially toxic ingestion, symptomatic patients, and those with suspected methanol intoxication with an anion gap metabolic acidosis or an osmolal gap greater than 10 mOsm should be treated with ADH inhibition. Folate should also be intravenously administered to patients requiring ADH inhibition. In patients who receive ADH inhibition who have a significant methanol concentration, consider hemodialysis since the apparent half-life of methanol under these circumstances is quite prolonged.
Clinical effect 1: Ataxia
Clinical effect 2: Drowsiness/lethargy
Clinical effect 3: Disinhibition
Clinical effect 4: Abdominal pain
Clinical effect 5: Nausea
Clinical effect 6: Vomiting
Clinical effect 7: Headache
Poisoning cause: Moderate Methanol toxicity
Toxic dose : The minimum toxic dose of methanol is approximately 100 mg/kg​​
Toxic serum or urine levels: Over 40 mg/dL
Management: Obtain a methanol level, serum chemistry, and a serum pH. A thorough visual exam should be performed, including visual acuity. An elevated osmolar gap suggests the presence of methanol or another alcohol but cannot be used to rule out a significant exposure. If a methanol concentration is readily available (results known within 2 hours) and the patient is asymptomatic, then alcohol dehydrogenase (ADH) inhibition can be delayed until the methanol concentration is available. Patients with a methanol concentration of more than 25 mg/dL or metabolic acidosis should be treated with ADH inhibition. If methanol concentrations cannot readily be measured, patients with a history of a potentially toxic ingestion, symptomatic patients, and those with suspected methanol intoxication with an anion gap metabolic acidosis or an osmolal gap greater than 10 mOsm should be treated with ADH inhibition. Folate should also be intravenously administered to patients requiring ADH inhibition. In patients who receive ADH inhibition who have a significant methanol concentration, consider hemodialysis since the apparent half-life of methanol under these circumstances is quite prolonged.
Clinical effect 1: Ataxia
Clinical effect 2: Drowsiness/lethargy
Clinical effect 3: Agitation/Irritability/Restlessness
Clinical effect 4: Abdominal pain
Clinical effect 5: Nausea
Clinical effect 6: Vomiting
Clinical effect 7: Headache
Clinical effect 8: Acidosis
Clinical effect 9: Visual impairment
Poisoning cause: Mild Acute Acetaminophen Toxicity
Toxic dose : Over 200 mg/kg (acute), 150 mg/kg (acute on chronic)
Toxic serum or urine levels: For evaluating acetaminophen level (APAP LEVEL, Tylenol level): consider the reported APAP level in the note and time post ingestion as ” time”and use this formula to calculate the toxic APAP level for that time. If time is between 4-24 hours you MUST do this calculation:
    if 4 <= time <= 24:
        line200 = round (math.exp(5.298317 - ((time - 4) * 0.1732868)))
        line150 = round(line200 - (0.25 * line200))
Management: ORAL: Obtain an acetaminophen concentration, 4 hours after ingestion or as soon as possible thereafter. If the time of ingestion is known and the acetaminophen concentration is measured between 4 and 24 hours postingestion, the patient can be risk stratified using the Rumack-Matthew Nomogram. If it is not possible to measure the serum acetaminophen concentration in a timely manner (results available within 8 hours of ingestion), and the amount ingested is either 200 mg/kg or more, or 10 g or more, whichever is less, start treatment with acetylcysteine . Patients who have an acetaminophen concentration above the treatment line (the line starting at 150 mcg/mL at 4 hours) should be treated with acetylcysteine. Patients who present with a history suggestive of acetaminophen exposure and an unknown time of ingestion should be treated with acetylcysteine if they have a detectable serum acetaminophen concentration OR if they have elevated serum transaminases.
Clinical effect 1: Asymptomatic
Clinical effect 2: Nausea
Clinical effect 3: Vomiting
Clinical effect 4: Abdominal pain
Clinical effect 5: Mild Elevation of serum transaminase (Alt,Ast<100)
Poisoning cause: Moderate Acute Acetaminophen Toxicity
Toxic dose : Over 200 mg/kg (acute), 150 mg/kg (acute on chronic)
Toxic serum or urine levels: For evaluating acetaminophen level (APAP LEVEL, Tylenol level): consider the reported APAP level in the note and time post ingestion as ” time”and use this formula to calculate the toxic APAP level for that time. If time is between 4-24 hours you MUST do this calculation:
    if 4 <= time <= 24:
        line200 = round (math.exp(5.298317 - ((time - 4) * 0.1732868)))
        line150 = round(line200 - (0.25 * line200))
Management: ORAL: Obtain an acetaminophen concentration, 4 hours after ingestion or as soon as possible thereafter. If the time of ingestion is known and the acetaminophen concentration is measured between 4 and 24 hours postingestion, the patient can be risk stratified using the Rumack-Matthew Nomogram. If it is not possible to measure the serum acetaminophen concentration in a timely manner (results available within 8 hours of ingestion), and the amount ingested is either 200 mg/kg or more, or 10 g or more, whichever is less, start treatment with acetylcysteine . Patients who have an acetaminophen concentration above the treatment line (the line starting at 150 mcg/mL at 4 hours) should be treated with acetylcysteine. Patients who present with a history suggestive of acetaminophen exposure and an unknown time of ingestion should be treated with acetylcysteine if they have a detectable serum acetaminophen concentration OR if they have elevated serum transaminases.
Clinical effect 1: Asymptomatic
Clinical effect 2: Nausea
Clinical effect 3: Vomiting
Clinical effect 4: Abdominal pain
Clinical effect 5: Mild Elevation of serum transaminase (Alt,Ast<100)
Clinical effect 6: Significant elevation of serum transaminase>1000
Poisoning cause: Severe Acute Acetaminophen Toxicity
Toxic dose : Over 200 mg/kg (acute), 150 mg/kg (acute on chronic)
Toxic serum or urine levels: For evaluating acetaminophen level (APAP LEVEL, Tylenol level): consider the reported APAP level in the note and time post ingestion as ” time”and use this formula to calculate the toxic APAP level for that time. If time is between 4-24 hours you MUST do this calculation:
    if 4 <= time <= 24:
        line200 = round (math.exp(5.298317 - ((time - 4) * 0.1732868)))
        line150 = round(line200 - (0.25 * line200))
Management: 1) Patients who present late after an acute acetaminophen ingestion (greater than 36 hours) may have significant liver injury and even liver failure (INR greater than 1.5, acidosis or encephalopathy). Intubate patients with altered mental status and resuscitate hypotensive patients with crystalloid and adrenergic vasopressors. Treat coagulopathic patients who are bleeding with fresh frozen plasma. Patients with renal failure may require renal replacement therapy. Administer intravenous acetylcysteine to all patients with liver injury. Patients with hepatic encephalopathy, acidosis or significant coagulopathy (INR greater than 5) should be evaluated for liver transplantation.
2) ORAL: Patients who present early following a massive ingestion (serum acetaminophen concentration greater than 500 mcg/mL) may have coma, metabolic acidosis, and hyperglycemia with normal serum transaminases. These patients generally recOver with supportive care (airway management, fluid resuscitation) and early acetylcysteine therapy.
Clinical effect 1: Liver failure
Clinical effect 2: Coagulopathy
Clinical effect 3: Delirium/encephalopathy
Clinical effect 4: Renal injury
Clinical effect 5: Coma
Clinical effect 6: Hyperglycemia
Clinical effect 7: Methemoglobinemia
Clinical effect 8: Lactic acidosis
Clinical effect 9: Significant elevation of serum transaminase>1000
Poisoning cause: Mild to Moderate Acetaminophen-Repeated Supratherapeutic Toxicity
Management: 1) Stop acetaminophen therapy. The vast majority of repeated supratherapeutic ingestions of acetaminophen can be managed with symptomatic and supportive care. Treatment should be initiated with n-acetylcysteine (NAC) if the patient’s acetaminophen concentration is greater than or equal to 20 mcg/mL and/or if liver enzymes are elevated. Patients should be treated until NAC stopping criteria are met. After completion of a FDA-approved or otherwise published NAC protocol, an acetaminophen concentration should be checked along with liver enzymes. Consensus guidelines recommend the following criteria for stopping NAC therapy: acetaminophen concentration less than 10 mcg/mL, INR less than 2, ALT/AST is normal or has decreased from its peak by 25% to 50% if elevated, and the patient is clinically well; however, if all the prior criteria are not met, NAC must be continued.
Clinical effect 1: Asymptomatic
Clinical effect 2: Alt elevation
Clinical effect 3: Malaise
Clinical effect 4: Nausea
Clinical effect 5: Vomiting
Clinical effect 6: Abdominal pain
Clinical effect 7: Mild Elevation of serum transaminase (Alt,Ast<100)
Clinical effect 9: Bilirubin increased
Clinical effect 10: Other LFTss abnormality
Poisoning cause: Severe Acetaminophen-Repeated Supratherapeutic Toxicity
Management:  Aggressive symptomatic and supportive care in addition to n-acetylcysteine therapy must be undertaken in severe toxicity. Intubate patients with respiratory compromise or encephalopathy. Maintain blood pressure with IV fluids and pressors if needed. Call your local poison center and or transplant team for assistance to help you decipher if your patient meets criteria for transplant.
Clinical effect 1: Jaundice
Clinical effect 2: Hypoglycemia
Clinical effect 3: Coagulopathy
Clinical effect 4: Renal failure
Clinical effect 5: Fulminant hepatic failure
Clinical effect 6: Delirium/encephalopathy
Clinical effect 7: Right upper quadrant pain
Clinical effect 8: Liver enlargement
Clinical effect 9: Oliguria
Clinical effect 10: Elevated bilirubin
Clinical effect 11: Mild Elevation of serum transaminase (Alt,Ast<100)
Clinical effect 12: Significant elevation of serum transaminase>1000
Clinical effect 13: Prolonged prothrombin time(pt)
Clinical effect 14: Anorexia
Clinical effect 15: Nausea
Clinical effect 16: Vomiting
Clinical effect 17: Malaise
Clinical effect 18: Cardiomyopathy
Poisoning cause: Mild to Moderate Oral/Parenteral Toothpaste or Fluoride Exposure
Toxic dose : Over 3-5 mg/kg.Vomiting and abdominal pain are common with ingestions of 3 to 5 mg/kg of elemental fluoride. Hypocalcemia and muscular symptoms may appear with 5 to 10 mg/kg. 
Management:  Most patients with dermal exposure will do well if irrigated immediately. There is no evidence that any products are more effective than water. Patients with ophthalmic exposure should have each eye irrigated with 1 L of normal saline, LR or water.
Clinical effect 1: Abdominal pain
Clinical effect 2: Nausea
Clinical effect 3: Vomiting
Poisoning cause: Severe Ocular Toothpaste or Fluoride Exposure
Management: Patients with ophthalmic exposure should have each eye irrigated with 1 L of normal saline, LR or water.
Clinical effect 1: Burns 
Clinical effect 2: Conjunctival ischemia
Clinical effect 3: Chemosis