SalioSAM/toxsample11 huggingface dataset:
Poisoning cause: ZIMELDINE toxicity
Management: Treatment is symptomatic and supportive. Monitor vital signs regularly. Manage mild hypotension with IV fluids. 
Clinical effect 1: Dizziness
Clinical effect 2: Drowsiness/lethargy
Clinical effect 3: Nausea
Clinical effect 4: Vomiting
Clinical effect 5: Seizure
Clinical effect 6: Abdominal pain
Clinical effect 7: Nystagmus
Clinical effect 8: Tremor
Clinical effect 9: PR prolongation
Clinical effect 10: Tachycardia
Clinical effect 11: Mild Elevation of serum transaminase (Alt,Ast<100)
Poisoning cause: MILD TO MODERATE Lamotrigine (Lamictal) TOXICITY
Toxic dose : 6 months - 79 years:	≥7.5 mg/kg.the toxic dose of Lamotrigine (Lamictal) might  occurs at doses > 200-500 mg
Toxic serum or urine levels: >30 mg/L
Management: Management will primarily be symptomatic and supportive. Manage mild hypotension with IV fluids
Clinical effect 1: Nausea
Clinical effect 2: Vomiting
Clinical effect 3: Anorexia
Clinical effect 4: Abdominal pain
Clinical effect 5: Drowsiness/lethargy
Clinical effect 7: Slurred speech
Clinical effect 8: Xerostomia
Clinical effect 9: Visual impairment
Clinical effect 10: Diplopia
Clinical effect 11: Skin rashes
Clinical effect 12: Confusion
Clinical effect 13: Nystagmus
Clinical effect 14: Ataxia
Clinical effect 15: Tremor
Clinical effect 16: Agitation/Irritability/Restlessness
Clinical effect 17: Dyskinesia
Clinical effect 18: Hyperreflexia
Clinical effect 20: Moderate Elevation of serum transaminase (100<ALT,AST<1000 )
Poisoning cause: SEVERE Lamotrigine (Lamictal) TOXICITY
Toxic dose :  probably >25 mg/kg
Management: Treatment is symptomatic and supportive. Closely monitor neurologic function. Treat seizures with IV benzodiazepines; barbiturates or propofol may be needed if seizures persist or recur. Manage hypotension with IV fluids and pressors if needed. Treat hypokalemia with oral or IV potassium chloride. Consider intravenous lipid therapy early for patients with ventricular dysrhythmias or hypotension
Clinical effect 1: Tachycardia
Clinical effect 2: Conduction disturbances/AV block
Clinical effect 3: Hypokalemia
Clinical effect 4: Oculogyric crisis
Clinical effect 5: Seizure
Clinical effect 6: Rhabdomyolysis
Clinical effect 7: Delirium/encephalopathy
Clinical effect 8: Coma
Clinical effect 9: Respiratory depression
Poisoning cause: MILD TO MODERATE haloperidol TOXICITY
Toxic dose : 6 months - 3 years:	>0.05 mg/kg OR >0.5 mg,
4 years - 17 years:	>0.05 mg/kg OR >3 mg,
18 years - 64 years:	>15 mg,
65 years - 79 years:	>2 mg
Management: Supportive care is the mainstay of treatment for butyrophenone toxicity. Evaluate for co-ingestants, intravenous fluids for volume expansion, and benzodiazepines for agitation or delirium. Treat significant extrapyramidal symptoms with anticholinergic agents. Benztropine or diphenhydramine for acute dystonia.
Clinical effect 1: CNS depression
Clinical effect 2: Drowsiness/lethargy
Clinical effect 3: Dystonia
Poisoning cause: SEVERE haloperidol TOXICITY
Toxic dose : 6 months - 3 years:	>0.05 mg/kg OR >0.5 mg,
4 years - 17 years:	>0.05 mg/kg OR >3 mg,
18 years - 64 years:	>15 mg,
65 years - 79 years:	>2 mg
Management: If CNS depression is severe, intubation and ventilation may be required to protect the airway. Intravenous fluid expansion is initial therapy for hypotension, and vasopressors may also be used if hypotension persists. For agitation and delirium, benzodiazepines should be given. If severe psychomotor agitation and hyperthermia develop, or other signs of NMS, sedation, intubation, and external cooling should be initiated. For QTc prolongation, ensure electrolytes are corrected and monitor for torsades de pointes
Clinical effect 1: Coma
Clinical effect 3: Delirium
Clinical effect 4: Agitation/Irritability/Restlessness
Clinical effect 5: Psychosis
Clinical effect 6: Hallucinations
Clinical effect 7: Hyperthermia
Clinical effect 8: Seizure
Clinical effect 9: Hypotension
Clinical effect 10: Torsades de pointes
Clinical effect 11: Neuroleptic malignant syndrome (NMS)
Clinical effect 13: Autonomic dysfunction
Clinical effect 14: Muscle rigidity
Clinical effect 15: CNS depression
Poisoning cause: MILD TO MODERATE ziprasidone(Geodon) TOXICITY
Toxic dose : 6 months - 11 years:	>80 mg,
12 years - 79 years:	>100 mg
Management: Treatment is symptomatic and supportive. Manage mild hypotension with IV fluids. Control agitation and confusion with benzodiazepines. 
Clinical effect 1: Nausea
Clinical effect 2: Vomiting
Clinical effect 3: Diarrhea
Clinical effect 4: Drowsiness/lethargy
Clinical effect 5: Agitation/Irritability/Restlessness
Clinical effect 6: Dizziness
Clinical effect 7: Slurred speech
Clinical effect 8: Extrapyramidal symptoms
Clinical effect 9: Dystonia
Clinical effect 10: Akathisia
Clinical effect 11: Dyskinesia
Poisoning cause: SEVERE ziprasidon(Geodon) TOXICITY
Toxic dose : 6 months - 11 years:	>80 mg,
12 years - 79 years:	>100 mg
Management: Treatment is symptomatic and supportive. Treat agitation with benzodiazepines. Treat seizures with IV benzodiazepines; barbiturates or propofol may be needed if seizures persist or recur. If hypotension is unresponsive to IV fluids, agents with alpha adrenergic effects, such an norepinephrine or phenylephrine, may be preferred. Agents with beta adrenergic activity, such as epinephrine or dopamine, may worsen hypotension in the setting of ziprasidone-induced alpha blockade. Manage severe extrapyramidal symptoms with anticholinergics and/or benzodiazepines. Therapeutic doses of ziprasidone may cause prolongation of the QT interval. Concomitant use of ziprasidone 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. Treat QRS prolongation or ventricular dysrhythmias with sodium bicarbonate; use lidocaine if sodium bicarbonate is unsuccessful. CardiOvert unstable ventricular dysrhythmias. Although rare, treat neuroleptic malignant syndrome with benzodiazepines, bromocriptine, consider dantrolene, as well as cooling and supportive measures.
Clinical effect 1: Hypotension
Clinical effect 2: Hypertension
Clinical effect 3: Tachycardia
Clinical effect 4: QRS widening
Clinical effect 5: Prolonged qtc
Clinical effect 6: Torsades de pointes
Clinical effect 7: Respiratory depression
Poisoning cause: MILD TO MODERATE clozapine TOXICITY
Toxic dose : Children under 12 should get care after ingesting Over 50mg, those 12+ after> 62.5mg, and regular users after 5x their single dose.
Management: The majority of clozapine Overdoses require only supportive care. Administer activated charcoal if patients can protect their airway and if they present shortly after ingestion. Mild sedation is common. Hypotension and tachycardia are generally mild and well tolerated, and do not require specific treatment except IV fluids
Clinical effect 1: Drowsiness/lethargy
Clinical effect 2: Anticholinergic symptoms
Clinical effect 3: Tachycardia
Clinical effect 4: Hypotension
Clinical effect 5: Nausea
Clinical effect 6: Vomiting
Clinical effect 7: Miosis
Clinical effect 8: Agitation/Irritability/Restlessness
Clinical effect 9: Nystagmus
Clinical effect 10: Ataxia
Clinical effect 11: Confusion
Clinical effect 12: Hallucinations
Poisoning cause: SEVERE clozapine TOXICITY
Toxic dose : Children under 12 should get care after ingesting Over 50mg, those 12+ after> 62.5mg, and regular users after 5x their single dose.
Management: Orotracheal intubation for airway protection should be performed early. Patients with laryngeal dystonia may require intubation and mechanical ventilation until symptoms resolve. Administer activated charcoal in patients who can protect their airway or who are intubated. Severe delirium may develop and require large doses of benzodiazepines for sedation. Seizures (which may progress to status epilepticus) may require aggressive use of benzodiazepines, propofol and/or barbiturates. Monitor core temperature and treat hyperthermia with external cooling and with aggressive benzodiazepine sedation to control agitation. Clinical manifestations may be prolonged due to prolonged absorption in the setting of anticholinergic ileus. Agranulocytosis is a potentially life-threatening complication of clozapine use, but it does not appear to be dose-related. Care is largely symptomatic and supportive, including administration of granulocyte colony stimulating factors.
Clinical effect 1: Delirium
Clinical effect 2: Seizure
Clinical effect 3: Coma
Clinical effect 4: Hyperthermia
Clinical effect 5: Hypotension
Clinical effect 6: Myoclonus
Clinical effect 7: Muscle rigidity
Clinical effect 8: Renal failure
Clinical effect 9: Ventricular dysrhythmia
Clinical effect 10: Prolonged qtc
Clinical effect 11: Rhabdomyolysis
Poisoning cause: MILD TO MODERATE NICOTINE TOXICITY
Toxic dose : CIGARETTE INGESTION: Anyone with an intentional ingestion, symptoms other than vomiting, or children who have ingested more than 1 cigarette or 3 or more cigarette butts should be evaluated in a health care facility. 
Management: Treatment is primarily supportive and symptomatic. Vomiting is common, which tends to limit absorption. Intravenous fluids can be administered. Persistent vital sign abnormalities, altered mental status, muscle weakness, and seizures indicate a more severe poisoning
Clinical effect 1: Abdominal pain
Clinical effect 2: Nausea
Clinical effect 3: Vomiting
Clinical effect 4: Dizziness
Clinical effect 5: Headache
Clinical effect 6: Tremor
Clinical effect 7: Diaphoresis
Clinical effect 8: Tachycardia
Clinical effect 9: Pallor
Clinical effect 10: Hypertension
Poisoning cause: SEVERE NICOTINE TOXICITY
Toxic dose : CIGARETTE INGESTION: Anyone with an intentional ingestion, symptoms other than vomiting, or children who have ingested more than 1 cigarette or 3 or more cigarette butts should be evaluated in a health care facility. Severe toxicity has been observed in children with doses as low as 2 mg. An estimated lethal dose is between 40 to 60 mg, but effects can be seen with much smaller amounts, especially in children.
Management: Treatment is primarily symptomatic and supportive. Patients may need airway support and mechanical ventilation for altered mental status, respiratory distress, secretions or respiratory paralysis. Atropine can be given for bradycardia or significant muscarinic signs (ie, bronchorrhea), if present. Hypotension should be treated with intravenous fluids and then a vasopressor as needed. Benzodiazepines should be used to treat seizures or severe agitation. Death is primarily from respiratory failure
Clinical effect 1: Seizure
Clinical effect 2: Confusion
Clinical effect 3: Weakness
Clinical effect 4: Bradycardia
Clinical effect 5: Hypotension
Clinical effect 6: Respiratory paralysis
Poisoning cause: Mild to moderate heroin toxicity
Toxic dose : >0 mg
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: Miosis
Poisoning cause: Severe heroin toxicity
Toxic dose : >0 mg
Management: 1) 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. Very high doses are rarely needed, but may be necessary in Overdoses of high potency opioids, like fentanyl. 2) A CONTINUOUS infusion may be necessary in patients that have ingested a long-acting opioid. A suggested starting rate is two-thirds of the dose effective for initial reversal that is administered each hour; titrate as needed. DURATION of effect is usually 1-2 hours. Many opioids have a much longer duration of effect, so it may be necessary to observe the patient at least 3-4 hours after the last dose of naloxone to ensure that the patient does not have recurrent symptoms of toxicity. Naloxone can precipitate withdrawal in an opioid-dependent patients, which is usually not life-threatening; however it can be extremely uncomfortable for the patient
Clinical effect 1: Respiratory depression
Clinical effect 2: Apnea
Clinical effect 3: Hypoxia
Clinical effect 4: Coma
Clinical effect 5: Bradycardia
Clinical effect 6: Seizure
Clinical effect 7: Acute lung injury
Clinical effect 8: Acute tubular necrosis
Clinical effect 9: Myoglobinuria
Clinical effect 10: Death
Poisoning cause: Mild oral acid toxicity
Management: Within the first 12 hours of exposure, if burns are absent or grade I severity, patient may be discharged when able to tolerate liquids and soft foods by mouth. If mild grade II burns, admit for intravenous fluids, slowly advance diet as tolerated. Perform barium swallow or repeat endoscopy several weeks after ingestion (sooner if difficulty swallowing) to evaluate for stricture formation
Clinical effect 1: Irritation or grade i burns (superficial hyperemia and edema) of the oropharynx,Esophagus,Or stomach
Poisoning cause: Moderate oral acid toxicity
Management: Within the first 12 hours of exposure, if burns are absent or grade I severity, patient may be discharged when able to tolerate liquids and soft foods by mouth. If mild grade II burns, admit for intravenous fluids, slowly advance diet as tolerated. Perform barium swallow or repeat endoscopy several weeks after ingestion (sooner if difficulty swallowing) to evaluate for stricture formation
Clinical effect 1: Grade II burns(blisters, erosions and ulcerations)
Poisoning cause: Severe oral acid toxicity
Management: Resuscitate with 0.9% saline; blood products may be necessary. Early airway management in patients with upper airway edema or respiratory distress. Early (within 12 hours) gastrointestinal endoscopy to evaluate for burns. Early bronchoscopy in patients with respiratory distress or upper airway edema. Early surgical consultation for patients with severe grade II or grade III burns, large deliberate ingestions, or signs, symptoms or laboratory findings concerning for tissue necrosis or perforation
Clinical effect 1: Deep burns
Clinical effect 2: Necrosis of the gastrointestinal mucosa
Clinical effect 3: GI perforation
Clinical effect 4: Fistula formation
Clinical effect 5: GI bleeding
Clinical effect 6: Upper airway edema
Clinical effect 7: Hypotension
Clinical effect 8: Tachycardia
Clinical effect 9: Tachypnea
Poisoning cause: Mild to moderate sodium chloride toxicity
Management: Dilute with milk or water. 
Clinical effect 1: Nausea
Clinical effect 2: Vomiting
Clinical effect 3: Diarrhea
Clinical effect 4: Abdominal pain
Clinical effect 5: Excessive thirst
Poisoning cause: Severe sodium chloride toxicity
Management: Treat hypernatremia with an IV solution containing 30 to 50 mEq/L sodium. Longstanding hypernatremia should be corrected slowly. Treat seizures with benzodiazepines. Treat cerebral edema with mannitol. Hemodialysis should be performed in patients with severe toxici
Clinical effect 1: Restlessness
Clinical effect 2: Seizure
Clinical effect 3: CNS depression
Clinical effect 4: Coma
Clinical effect 5: Hypotension
Clinical effect 6: Respiratory arrest
Clinical effect 7: Acute ulcerative gastritis
Clinical effect 8: Hypernatremia
Clinical effect 9: Hyperchloremia
Clinical effect 10: Fluid retention
Clinical effect 11: Pulmonary edema
Clinical effect 12: Cerebral edema
Clinical effect 13: Hyperosmolarity of cerebral fluids
Clinical effect 14: Cellular crenation
Clinical effect 15: Irreversible neurologic damage
Poisoning cause: Mild to moderate oral ammonia toxicity (ammonia ingestion)
Management: Perform early (within 12 hours) endoscopy in patients with stridor, drooling, vomiting, significant oral burns, difficulty swallowing or abdominal pain, and in all patients with deliberate ingestion. If burns are absent or grade I severity, patient may be discharged when able to tolerate liquids and soft foods by mouth. If mild grade II burns, admit for intravenous fluids, slowly advance diet as tolerated. Perform barium swallow or repeat endoscopy several weeks after ingestion (sooner if difficulty swallowing) to evaluate for stricture formation.
Clinical effect 1: Irritation
Clinical effect 2: Grade i burns (superficial hyperemia and edema) of oropharynx
Clinical effect 3: Esophagus
Clinical effect 4: Or stomach
Clinical effect 5: Potential upper airway edema
Poisoning cause: Severe oral ammonia toxicity
Management: Resuscitate with 0.9% saline; blood products may be necessary. Early airway management in patients with upper airway edema or respiratory distress. Early (within 12 hours) gastrointestinal endoscopy to evaluate for burns. Early bronchoscopy in patients with respiratory distress or upper airway edema. Early surgical consultation for patients with severe grade II or grade III burns, large deliberate ingestions, or signs, symptoms or laboratory findings concerning for tissue necrosis or perforation
Clinical effect 1: Deep burns
Clinical effect 2: Necrosis of gastrointestinal mucosa
Clinical effect 3: GI  perforation
Clinical effect 4: Fistula formation
Clinical effect 5: GI bleeding
Clinical effect 6: Upper airway edema
Clinical effect 7: Hypotension
Clinical effect 8: Tachycardia
Clinical effect 9: Tachypnea
Clinical effect 10: Fever
Clinical effect 11: Long-term GI stricture formation
Clinical effect 12: Esophageal carcinoma
Poisoning cause: Mild to moderate local anesthetic toxicity
Management: Supportive care is the mainstay of treatment in mild to moderate toxicity. Paresthesias and paralysis resolve in virtually all cases. Anxiety can be managed with benzodiazepines. Patients with significant oropharyngeal anesthesia should be positioned upright with nothing by mouth (NPO) to avoid aspiration
Clinical effect 1: Drowsiness/lethargy
Clinical effect 2: Impending doom
Clinical effect 3: Headache
Clinical effect 4: Dizziness
Clinical effect 5: Paresthesias
Clinical effect 6: Euphoria
Clinical effect 7: Numbness of the mouth
Clinical effect 8: Lightheadedness
Clinical effect 9: Tinnitus
Clinical effect 10: Anxiety
Clinical effect 11: Confusion
Clinical effect 12: Tremors
Clinical effect 13: Agitation/Irritability/Restlessness
Clinical effect 14: Disorientation
Clinical effect 15: Hallucinations
Clinical effect 16: Lethargy
Clinical effect 17: Temporary paralysis
Clinical effect 18: Suppression of the gag reflex
Clinical effect 19: Methemoglobinemia
Poisoning cause: Severe local anesthetic toxicity
Management: Patients with severe toxicity (eg, depressed mental status, seizures, hypotension, dysrhythmias, cardiac arrest) should receive standard supportive care (intubation and mechanical ventilation, intravenous fluids and pressors for hypotension, benzodiazepines for seizures). Consider intravenous lipid therapy early for patients with ventricular dysrhythmias or hypotension. ANTIDOTE 1) METHEMOGLOBINEMIA: Initiate oxygen therapy. Treat with methylene blue if patient is symptomatic (usually at methemoglobin concentrations greater than 20% to 30% or at lower concentrations in patients with anemia, underlying pulmonary or cardiovascular disease). METHYLENE BLUE: INITIAL DOSE/ADULT OR CHILD: 1 mg/kg IV Over 5 to 30 minutes; a repeat dose of up to 1 mg/kg may be given 1 hour after the first dose if methemoglobin levels remain greater than 30% or if signs and symptoms persist. NOTE: Methylene blue is available as follows: 50 mg/10 mL (5 mg/mL or 0.5% solution) single-dose ampules and 10 mg/1 mL (1% solution) vials. Additional doses may sometimes be required. Improvement is usually noted shortly after administration if diagnosis is correct. Consider other diagnoses or treatment options if no improvement has been observed after several doses. If intravenous access cannot be established, methylene blue may also be given by intraosseous infusion. Methylene blue should not be given by subcutaneous or intrathecal injection. NEONATES: DOSE: 0.3 to 1 mg/kg
Clinical effect 1: Methemoglobinemia
Clinical effect 2: Hypotension
Clinical effect 3: Av block
Clinical effect 4: Bradycardia
Clinical effect 5: Qrs prolongation
Clinical effect 6: Ventricular dysrhythmias
Clinical effect 7: Asystole
Clinical effect 8: Cardiac arrest
Clinical effect 9: Respiratory depression
Clinical effect 10: Hypoxia
Poisoning cause: Cephalosporin Overdose
Management: Nausea, vomiting, diarrhea, abdominal pain, seizure
Clinical effect 1: Nausea
Clinical effect 2: Vomiting
Clinical effect 3: Diarrhea
Clinical effect 4: Abdominal pain
Clinical effect 5: Seizure
Poisoning cause: Dapsone toxicity
Toxic dose : 6 months - 35 months:	>0 mg,
3 years - 11 years:	>1 mg/kg OR >50 mg,
12 years - 17 years:	>1 mg/kg OR >100 mg,
18 years - 54 years:	>100 mg,
55 years - 79 years:	>50 mg
Management: Treatment is largely supportive, intravenous fluids and antiemetics may be necessary for patients with persistent vomiting. Symptomatic methemoglobinemia should be treated with methylene blue
Clinical effect 1: Hemolytic anemia
Clinical effect 2: Methemoglobinemia
Clinical effect 3: Sulfhemoglobinemia
Clinical effect 4: Tachycardia
Clinical effect 5: Hypertension
Clinical effect 6: Agitation/Irritability/Restlessness
Clinical effect 7: Hallucinations
Clinical effect 8: Confusion
Clinical effect 9: Nausea
Clinical effect 10: Vomiting
Clinical effect 11: Diarrhea
Clinical effect 12: Hepatotoxicity
Clinical effect 13: Hematuria
Clinical effect 14: Peripheral neuropathy
Clinical effect 15: Cold perspiration
Clinical effect 16: Blue-gray cyanosis
Poisoning cause: Mild to moderate isoniazid toxicity
Toxic dose : <50 kg:	>10 mg/kg OR >300 mg
≥50 kg:	>15 mg/kg OR >900 mg
Toxic serum or urine levels: >10 mg/kg OR >300 mg
Management: Patients who present within 2 hours after a large ingestion should be given a prophylactic dose of pyridoxine. Intravenous access should be established and the patient should be placed in a resuscitation-ready room. Seizures may be the presenting sign of ingestion and represent a more severe poisoning
Clinical effect 1: Vomiting
Clinical effect 2: Slurred speech
Clinical effect 3: Dizziness
Clinical effect 4: Tachycardia