SalioSAM/toxsample11 huggingface dataset:
Poisoning cause: MILD TO MODERATE Ethanol TOXICITY
Toxic dose : About 1 mL/kg (1 g/kg) of absolute ethanol. Per Olson guidleine:Acute ingestion of 150-200 mg/kg can produce mild intoxication, 
Toxic serum or urine levels: Over 100 mg/dL
Management: Patients who appear mildly intoxicated may be simply managed with supportive care only. An ethanol concentration is generally not needed for management. Patients can be discharged when they are not clinically intoxicated (no ataxia, nystagmus, or slurred speech). Significant CNS depression indicates a more severe poisoning. 
Clinical effect 1: Euphoria
Clinical effect 2: Ataxia
Clinical effect 3: Nystagmus
Clinical effect 4: Disinhibition
Clinical effect 5: Aggressive behavior
Clinical effect 6: Nausea
Clinical effect 7: Vomiting
Clinical effect 8: Flushing
Clinical effect 9: Supraventricular tachyarrhythmias
Clinical effect 10: Atrial fibrillation
Poisoning cause: SEVERE Ethanol TOXICITY
Toxic dose :  5 to 6 g/kg in non-tolerant adults and 3 g/kg in children. Per Olson guidleine:Acute ingestion of  300-500 mg/kg can lead to severe intoxication. Chronic intoxication may occur with more than 100 mg/kg/day for 2 or more days​​.
Toxic serum or urine levels: Over 250- 400 mg/dL  
Management: Measure a serum ethanol level if ethanol is believed to be the cause of altered mental status, and consider and rule out other reversible causes of altered mental status, such as hypoglycemia, hypoxia, and opiate intoxication. Patients who are comatose may require airway protection. Other causes of altered mental status should be considered, because ethanol is often a coingestant with other drugs, and intoxicated patients are predisposed to traumatic injuries. Children may be susceptible to hypoglycemia following an ethanol ingestion. Alcoholic ketoacidosis is a condition that typically develops in chronic drinkers that results in impaired gluconeogenesis. It often develops after binge drinking combined with malnutrition. Vomiting, abdominal pain, and an anion-gap metabolic acidosis develop. Treatment is with fluid replacement and dextrose supplementation. Thiamine, folate, and other vitamins should also be provided intravenously. Ethanol withdrawal is a potentially life-threatening condition that may result in chronic drinkers following a period of abstinence. It usually begins with autonomic hyperactivity, tachycardia, tremor, hypertension, agitation leading to hallucinations, and seizures. Treatment is generally with benzodiazepines for sedation. In patients with resistant symptoms, consider the use of propofol or a barbiturate such as phenobarbital
Clinical effect 1: Coma
Clinical effect 2: Respiratory depression
Clinical effect 3: Pulmonary aspiration
Clinical effect 4: Hypoglycemia
Clinical effect 5: Hypothermia
Poisoning cause: Sudden cessation of chronic ethanol
Management: Mild to Moderate AWS:
Benzodiazepines are central to treatment, administered either orally or intravenously.
Aim to control withdrawal symptoms and prevent seizures.
For mild AWS, a long-acting benzodiazepine like clorazepate may be used, starting with 30 mg and then 15 mg 2 to 4 times daily, tapering Over 4-5 days.
Moderate AWS might require intravenous benzodiazepines such as lorazepam or diazepam.
Patients should also receive thiamine, multivitamins, and potassium and magnesium supplements if necessary.
Severe AWS:
Indications: Overt delirium tremens, significant agitation, disorientation, and notable autonomic dysfunction (e.g., tachycardia, Hypertension).
Aggressive intravenous benzodiazepine treatment is essential, aiming for rapid sedation.
Start with 2-4 mg of lorazepam or 5-10 mg of diazepam, titrating rapidly as needed. In severe cases, doses may be increased to 8-12 mg lorazepam or 20-40 mg diazepam every 15 minutes.
The treatment goal is to reduce tachycardia, hypertension, and tremors, achieving mild sedation (patient is calm but responsive).
If benzodiazepines don't control symptoms adequately, consider propofol at 0.5 to 1 mg/kg in repetitive doses.
Airway management might be needed for those with severe withdrawal.
Ensure fluid resuscitation in hypovolemic patients.
Clinical effect 1: Hypertension
Clinical effect 2: Tachycardia
Clinical effect 3: Tremors
Clinical effect 4: Seizure
Clinical effect 5: Delirium
Clinical effect 6: Hypothermia
Clinical effect 7: Hypotension
Clinical effect 8: Bradypnea
Clinical effect 9: Hyperventilation/tachypnea
Clinical effect 10: Acidosis
Poisoning cause: MILD TO MODERATE Arsenic TOXICITY
Toxic dose : Acute ingestion of more than  0.05 mg/kg,Acute ingestion of more than 100 mg of inorganic arsenic is likely to cause significant toxicity
Toxic serum or urine levels: Over 100 mcg/L
Management: Fluid resuscitation should be initiated immediately, but care must be taken to recognize pulmonary and cerebral edema when present. When a significant acute ingestion is confirmed, chelation therapy should be initiated immediately prior to laboratory confirmation. This will minimize time delay to treatment associated with prolonged laboratory result turn around. In chronic toxicity, the decision to chelate must be based upon patient condition and laboratory evaluation
Clinical effect 1: Rapid onset of gastrointestinal symptoms
Clinical effect 2: Oral burns (incl. lips)
Clinical effect 3: Abdominal pain
Clinical effect 4: Vomiting
Clinical effect 5: "rice water-like" diarrhea
Clinical effect 6: Dehydration
Clinical effect 7: Muscle cramps
Clinical effect 8: Facial swelling
Clinical effect 9: Bronchitis
Clinical effect 11: Electrolyte distrubances
Poisoning cause: Subacute Arsenic toxicity
Toxic serum or urine levels: Toxic Urine Arsenic = Over 100 mcg/L
Clinical effect 1: Peripheral neuropathy
Clinical effect 2: Resembling guillain-barre syndrome
Poisoning cause: SEVERE acute Arsenic TOXICITY
Toxic dose : Acute ingestion of more than 100-300 mg of inorganic arsenic is likely to cause significant toxicity.
Toxic serum or urine levels: Toxic Urine Arsenic = Over 100 mcg/L
Management: Aggressive life support measures should be instituted immediately. Anti-arrhythmic medications that prolong the QTc should be avoided. In severely ill patients, combined therapy with both BAL and an oral agent should be considered. If renal failure exists, the dose of BAL should be decreased after the loading dose. 
Clinical effect 1: Early signs are hypotension
Clinical effect 2: Tachycardia
Clinical effect 3: Fever/hyperthermia
Clinical effect 4: Hyperventilation/tachypnea
Clinical effect 5: Ventricular dysrhythmia
Clinical effect 6: Delirium/encephalopathy
Clinical effect 7: Seizure
Clinical effect 8: Coma
Clinical effect 9: Renal failure
Clinical effect 10: Hemolytic anemia
Clinical effect 11: Hepatitis
Poisoning cause: CHRONIC Arsenic TOXICITY
Toxic serum or urine levels: Toxic Urine Arsenic = Over 100 mcg/L
Clinical effect 1: Weakness
Clinical effect 2: Anorexia
Clinical effect 3: Hepatomegaly
Clinical effect 4: Jaundice
Clinical effect 5: Respiratory irritation
Clinical effect 6: Hyperpigmentation
Clinical effect 7: Dermatitis
Clinical effect 8: Peripheral neuropathies
Clinical effect 9: Skin cancer
Clinical effect 10: Lung cancer
Clinical effect 11: Bladder cancer
Clinical effect 12: Liver cancers
Poisoning cause: MILD TO MODERATE Phenobarbital TOXICITY
Toxic dose :  Ingestion of 8 mg/kg phenobarbital generally causes some CNS depression in non-tolerant individuals.Toxicity is likely when the dose exceeds 5–10 times the hypnotic dose. 
Toxic serum or urine levels: from 3 to 40 mcg/ml (lethargy and ataxia), from 60 to 150 mcg/ml (coma), 150 mcg/ml (hypotension and coma
Management: Activated charcoal may be given if patients present shortly after ingestion, and are awake and alertwith a protected airway
Clinical effect 1: Drowsiness/lethargy
Clinical effect 2: Slurred speech
Clinical effect 3: Nystagmus
Clinical effect 4: Confusion
Clinical effect 5: Ataxia
Poisoning cause: SEVERE Phenobarbital TOXICITY
Toxic dose :  Ingestion of 8 mg/kg phenobarbital generally causes some CNS depression in non-tolerant individuals.Toxicity is likely when the dose exceeds 5–10 times the hypnotic dose. 
Toxic serum or urine levels: from 3 to 40 mcg/ml (lethargy and ataxia), from 60 to 150 mcg/ml (coma), 150 mcg/ml (hypotension and coma
Management: Orotracheal intubation for airway protection should be performed if patient is increasingly drowsy or comatose. Administer activated charcoal (GI decontamination should be performed only in patients who can protect their airway or who are intubated). Severe hypotension and hypothermia may develop; aggressive supportive care is the mainstay of treatment including passive rewarming, administration of normal saline, and in severe cases vasopressors. QT interval prolongation may occur with IV phenobarbital sodium administration. In patients with QT prolongation, monitor serum electrolytes including potassium, calcium and magnesium in patients with significant Overdose; correct any abnormalities. Concomitant use of IV phenobarbital sodium and other drugs that prolong the QT interval may increase the risk of torsades de pointes. Treat torsades de pointes with IV magnesium sulfate, and correct electrolyte abnormalities, Overdrive pacing may be necessary. At the time of this review, torsades de pointes has not been reported with therapy. Overall, clinical manifestations may be prolonged due to long half-life of drug. Tetanus and routine wound care for blisters. A burn surgeon should be consulted for extensive skin blistering
Clinical effect 1: Coma
Clinical effect 2: Hypotension
Clinical effect 3: Decreased myocardial contractility
Clinical effect 4: Hypothermia
Clinical effect 5: Respiratory depression
Clinical effect 6: Blisters
Clinical effect 7: Miosis
Clinical effect 8: Diminished reflexes
Clinical effect 9: Respiratory depression
Clinical effect 10: Cardiovascular collapse
Clinical effect 11: Aspiration pneumonia
Clinical effect 12: Rhabdomyolysis
Clinical effect 13: Renal failure
Poisoning cause: MILD TO MODERATE Valproic acid TOXICITY
Toxic dose : Over 50 mg/kg
Toxic serum or urine levels: Over 100 mcg/ml
Management: Symptomatic and supportive care in all patients. Monitor for progression of sedation. Repeat valproic acid levels every 4 to 6 hours and consider multidose activated charcoal if the level is continuously rising.
Clinical effect 1: CNS depression
Clinical effect 2: Drowsiness/lethargy
Clinical effect 3: Vomiting
Clinical effect 4: Tachycardia
Poisoning cause: SEVERE Valproic acid TOXICITY
Toxic dose : Over 200 mg/kg
Toxic serum or urine levels: Serum levels exceeding 450 mg/L are associated with drowsiness or obtundation.
Levels greater than 850 mg/L are associated with coma, respiratory depression, and metabolic perturbations.
Management: Resuscitation, symptomatic and supportive care in all patients. Early intubation in patient with declining level of consciousness. Hypotension: Treat with IV fluids, if no response start vasopressors. Consider hemodialysis in patients with severe toxicity who are not responding to supportive care. Consider carnitine in patients with coma, hepatotoxicity, elevated ammonia concentration, or a valproate concentration above 450 mcg/mL. 
Clinical effect 1: Coma
Clinical effect 2: Miosis
Clinical effect 3: Tachycardia
Clinical effect 4: Hypotension
Clinical effect 5: QTc prolongation
Clinical effect 6: Respiratory depression
Clinical effect 7: Seizure
Clinical effect 8: Cerebral edema
Clinical effect 9: Hypernatremia
Clinical effect 10: Hypocalcemia
Clinical effect 11: Hyperammonemia
Clinical effect 12: Bone marrow suppression
Clinical effect 13: Pancreatitis
Clinical effect 14: Mild Elevation of serum transaminase (Alt,Ast<100)
Clinical effect 16: Bilirubin increased
Clinical effect 17: Other LFTs abnormality
Clinical effect 18: Renal insufficiency
Clinical effect 19: Lung injury
Clinical effect 20: Hyperammonemic encephalopathy
Clinical effect 21: Cognitive impairment
Clinical effect 22: Elevated ammonia
Clinical effect 23: Delirium/encephalopathy
Poisoning cause: MILD TO MODERATE Carbamazepine TOXICITY
Toxic dose : Over 10 mg/kg
Toxic serum or urine levels: Over 12 mg/L
Management: Treatment of mild to moderate toxicity is largely supportive. Sinus tachycardia should be treated with fluid resuscitation and benzodiazepines for anticholinergic symptoms. Dystonic reactions can be treated with anticholinergic medications, such as diphenhydramine 25 mg, or benzodiazepines if the patient is also exhibiting signs of anticholinergic toxicity (ie, mydriasis, delirium, flushing, dry mucous membranes, decreased bowel sounds, and urinary retention). Adverse reactions to chronic therapy such as transaminitis or cytopenia should be treated by discontinuation of the medication. 
Clinical effect 1: Nystagmus
Clinical effect 2: Ataxia
Clinical effect 3: Hyperreflexia
Clinical effect 4: CNS depression
Clinical effect 5: Dystonia
Clinical effect 6: Tachycardia
Clinical effect 7: Anticholinergic symptoms
Clinical effect 8: Mydriasis
Clinical effect 9: Delirium/encephalopathy
Clinical effect 10: Decreased bowel sounds
Poisoning cause: Severe Carbamazepine TOXICITY
Toxic dose : Over 10 mg/kg
Toxic serum or urine levels: Over 40 mg/L
Management: Supportive care is the mainstay of treatment. Specific interventions based on the system of toxicity are as follows: 
a) CNS: Mental status depression may require airway protection. Coma should be treated with airway management and supportive care. Seizures should be treated with benzodiazepines as first-line therapy followed by barbiturates or propofol. Agitated patients should be treated with benzodiazepines, large doses may be required. 
b) CARDIOVASCULAR: Hypotension should be treated with isotonic fluids. If unresponsive to 2 or more liters of fluid, vasopressor agents, such as norepinephrine or phenylephrine, should be administered. In rare cases, cardiopulmonary bypass or aortic balloon pump may be used to maintain perfusion while carbamazepine is metabolized. QRS widening (progressive widening on serial ECGs or a single ECG with a QRS duration longer than 140 msec) should be treated with sodium bicarbonate boluses of 50 mEq (CHILD: 1 to 2 mEq/kg of sodium bicarbonate) until the QRS narrows. The serum pH should be maintained between 7.4 and 7.55. 
c) RESPIRATORY: Intubation and mechanical ventilation should be considered for respiratory depression. 
d) GASTROINTESTINAL: Severe nausea and vomiting should be treated with antiemetics, preferably agents without additional anticholinergic activity (eg, ondansetron). 
e) RENAL: Urinary retention is due to anticholinergic effects and should be treated with catheterization. Urine output should be maintained above 30 mL/hr because the metabolites are primarily renally cleared. Acute renal failure is due to hypotension or rhabdomyolysis and should be treated with liberal fluid administration. 
Clinical effect 1: Coma
Clinical effect 2: Respiratory depression
Clinical effect 3: Rhabdomyolysis
Clinical effect 4: PR prolongation
Clinical effect 5: Renal failure
Clinical effect 6: Decreased myocardial contractility
Clinical effect 7: Pulmonary edema
Clinical effect 8: Hypotension
Clinical effect 9: Dysrhythmia
Clinical effect 10: QRS prolongation
Clinical effect 11: QTc prolongation
Clinical effect 12: Seizure
Poisoning cause: MILD TO MODERATE Theophylline TOXICITY
Toxic dose :  Acute overdose of more than 50 mg/kg may result in serum levels above 100 mg/L and can include symptoms like vomiting, tremor, anxiety, and tachycardia​​.
Toxic serum or urine levels: Over 40 mcg/ml (chronic), 80 mcg/ml (acute)
Management: Establish IV access and place the patient on a cardiac monitor. Treat nausea with an antiemetic and administer IV fluids. Monitor electrolytes
Clinical effect 1: Nausea
Clinical effect 2: Vomiting
Clinical effect 3: Abdominal pain
Clinical effect 4: Tachycardia
Clinical effect 5: Sustained complex atrial or ventricle ectopy
Clinical effect 6: Tremor
Clinical effect 7: Agitation/Irritability/Restlessness
Clinical effect 8: Hypokalemia
Clinical effect 9: Hyperglycemia
Clinical effect 10: Hypophosphatemia
Clinical effect 11: Hypocalcemia
Poisoning cause: SEVERE Theophylline TOXICITY
Toxic dose :  Acute overdose of more than 50 mg/kg may result in serum levels above 100 mg/L and can include symptoms like vomiting, tremor, anxiety, and tachycardia​​.
Toxic serum or urine levels: Over 40 mcg/ml (chronic), 80 mcg/ml (acute)
Management: The primary effect of theophylline is increased sympathomimetic effects. The primary treatment is sedation with benzodiazepines (such as lorazepam 1 to 2 mg IV every 5 min titrated to effect); high doses may be required. Hemodynamically significant tachycardia should be treated with esmolol, which can paradoxically improve blood pressure in severely tachycardic patients. Hypotension should be treated with IV fluids. Adrenergic vasopressors can theoretically make tachycardia worse, but there are numerous reports of successful treatment of severe toxicity with these agents. Vasopressin is of theoretical value and has been used effectively in a case of caffeine poisoning. Lidocaine administration has been associated with successful treatment of ventricular fibrillation. Hemodialysis should be performed in patients with severe toxicity, and patients with high serum theophylline concentrations (80 to 100 mcg/mL after acute Overdose, 40 to 60 mcg/mL with chronic toxicity). 
Clinical effect 1: Seizure
Clinical effect 2: Rhabdomyolysis
Clinical effect 3: Hypotension
Clinical effect 4: Ventricular dysrhythmia
Clinical effect 5: Acidosis
Clinical effect 6: Respiratory alkalosis
Poisoning cause: CHRONIC Theophylline TOXICITY
Toxic serum or urine levels: Over 40 mcg/ml (chronic), 80 mcg/ml (acute)
Management: The primary effect of theophylline is increased sympathomimetic effects. The primary treatment is sedation with benzodiazepines (such as lorazepam 1 to 2 mg IV every 5 min titrated to effect); high doses may be required. Hemodynamically significant tachycardia should be treated with esmolol, which can paradoxically improve blood pressure in severely tachycardic patients. Hypotension should be treated with IV fluids. Adrenergic vasopressors can theoretically make tachycardia worse, but there are numerous reports of successful treatment of severe toxicity with these agents. Vasopressin is of theoretical value and has been used effectively in a case of caffeine poisoning. Lidocaine administration has been associated with successful treatment of ventricular fibrillation. Hemodialysis should be performed in patients with severe toxicity, and patients with high serum theophylline concentrations (80 to 100 mcg/mL after acute Overdose, 40 to 60 mcg/mL with chronic toxicity). 
Clinical effect 1: Mild gastrointestinal symptoms
Clinical effect 2: Seizure
Clinical effect 3: Dysrhythmia
Poisoning cause: MILD TO MODERATE acute Lithium TOXICITY
Toxic dose :  Ingestion of 1 mEq/kg (40 mg/kg) can produce a blood level of approximately 1.2 mEq/L​​.
Toxic serum or urine levels: Over  4 mEq/L (acute)
Management: Most acute lithium Overdoses may be safely managed with supportive care that includes: antiemetics for nausea and vomiting, intravenous normal saline hydration to enhance renal lithium elimination, and correction of any electrolyte abnormalities
Clinical effect 1: Nausea
Clinical effect 2: Vomiting
Clinical effect 3: Diarrhea
Poisoning cause: MILD TO MODERATE chronic Lithium TOXICITY
Toxic serum or urine levels: Between 1.5 and 2.5 mEq/L(Chronic) (predicted outcome is mild effect),
Management:  For chronic toxicity, address underlying causes of decreased renal clearance, including intravenous fluids for dehydration or discontinuing medications that impair renal function.
Clinical effect 1: Nausea
Clinical effect 2: Vomiting
Clinical effect 3: Diarrhea
Clinical effect 4: Dehydration
Clinical effect 5: Nystagmus
Clinical effect 6: Tremors
Clinical effect 7: Hyperreflexia
Clinical effect 8: Cogwheel rigidity
Clinical effect 9: Ataxia
Clinical effect 10: Agitation/Irritability/Restlessness
Clinical effect 11: Confusion
Clinical effect 12: Drowsiness/lethargy
Clinical effect 13: Bradycardia
Clinical effect 14: T-wave abnormalities
Clinical effect 15: Hypoventilation
Poisoning cause: SEVERE chronic Lithium TOXICITY
Toxic serum or urine levels: 
Between 2.5 and 3.5 mEq/L (Chronic) (predicted outcome is moderate to severe effect),
Over 3.5 mEq/L (Chronic) (predicted outcome is severe effect).
Management: Orotracheal intubation for airway protection should be performed if recurrent seizures, increasing somnolence or coma develop. Administer intravenous normal saline to enhance renal elimination of lithium (Goal: urine output of 2 to 3 mL/kg/hr). Intravenous fluids and vasopressors (dopamine, norepinephrine) may be needed to treat hypotension. Treat agitation, rigidity, seizures, hyperthermia, serotonin syndrome with sedation (benzodiazepines, propofol), and cooling measures; intubation and paralysis may be necessary with severe toxicity. Consider hemodialysis for patients with severe toxicity not responding to hydration, or congestive heart failure or renal insufficiency. Dysrhythmias are treated with standard ACLS protocols.
Clinical effect 1: Photophobia
Clinical effect 2: Dehydration
Clinical effect 3: Electrolyte distrubances
Clinical effect 4: Thyroid dysfunction
Clinical effect 5: Hyperthermia
Clinical effect 6: Seizure
Clinical effect 7: Coma
Clinical effect 8: Rigidity
Clinical effect 9: Myoclonus
Clinical effect 10: Serotonin syndrome
Clinical effect 11: ECG changess
Clinical effect 12: Nonspecific t-wave abnormalities
Clinical effect 13: QTc prolongation
Clinical effect 14: Bundle branch block
Clinical effect 15: Bradycardia
Clinical effect 16: Junctional rhythm
Clinical effect 17: Hypotension
Clinical effect 18: Hypoventilation
Clinical effect 19: Respiratory depression
Clinical effect 20: ARDS
Clinical effect 21: Bezoars
Poisoning cause: Mild to Moderate Lead Toxicity
Toxic serum or urine levels: Over 5 mcg /dL
Management: The primary concerns of mild to moderate toxicity from lead exposure in young children are neurodevelopmental, specifically lower intelligence quotient scores and behavioral problems. Population studies suggest that mild cognitive impairment develops at low levels of lead exposure (blood lead concentrations of 10 mcg/dL). Intermittent vomiting, anorexia and abdominal pain may also develop. In mild to moderate exposures in adults, concerns include hypertension, spontaneous abortion and sperm abnormalities, and more subtle neurocognitive effects. Fatigue, mild somnolence, headache, insomnia, abdominal pain, constipation, mild anemia, myalgias and arthralgias, and mild weakness may also develop.
Clinical effect 1: Neurodevelopmental concerns in young children
Clinical effect 2: Lower intelligence quotient scores
Clinical effect 3: Behavioral problems
Clinical effect 4: Cognitive impairment
Clinical effect 5: Intermittent/persistent vomiting
Clinical effect 6: Vomiting
Clinical effect 7: Anorexia
Clinical effect 8: Abdominal pain
Clinical effect 9: Hypertension
Clinical effect 10: Spontaneous abortion
Clinical effect 11: Sperm abnormalities
Clinical effect 12: Subtle neurocognitive effects
Clinical effect 13: Fatigue
Clinical effect 14: Drowsiness/lethargy
Clinical effect 15: Headache
Clinical effect 16: Insomnia
Clinical effect 17: Constipation
Clinical effect 18: Anemia
Clinical effect 19: Myalgias
Clinical effect 20: Arthralgias
Clinical effect 21: Weakness