Questions and Answers
In the context of poison control calls, which statement is most accurate regarding exposure incidents?
What is the significance of the statistic regarding poison control calls for children?
What proportion of poison control calls in 2017 were related to children?
What was the total number of human exposure calls to poison control in 2017?
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Which demographic accounted for over 1 million of the poison control calls in 2017?
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What can be inferred about the population trends in poison control calls in 2017?
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Which organization is likely involved in tracking the statistics of poison control calls?
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Which of the following most accurately describes the nature of poison control calls in 2017?
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What is the main effect of organophosphates on acetylcholine receptors?
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Which of the following symptoms is NOT associated with a hypercholinergic response?
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Which treatment is used to deactivate the effects of organophosphates?
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Which component of the Mark 1 Kit is primarily responsible for blocking muscarinic receptors?
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What does the mnemonic SLUDGEM help remember?
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Which of the following substances is known to be contained in Lomotil and can be abused for narcotic effects?
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What characteristic symptom is associated with anticholinergic toxicity, particularly when accompanied by hyperthermia?
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Which clinical presentation is described as 'dry as a bone' in the context of anticholinergic effects?
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Which statement best describes the mechanism of action of anticholinergics?
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Which option lists a symptom associated with acute anticholinergic delirium?
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What major complication is associated with sympathomimetic use, especially in extreme cases?
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Which of the following is NOT recommended for treating sympathomimetic toxicity?
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What physiological changes are typically observed in a patient experiencing sympathomimetic intoxication?
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Which of the following treatments is specifically contraindicated in a patient with sympathomimetic toxicity?
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What potential complication arises from rhabdomyolysis due to sympathomimetic use?
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Which of the following substances is primarily associated with the hallmark symptom of miosis upon ingestion?
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What is a common mechanism of action shared by most sedative/hypnotic substances listed?
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Which treatment is specifically mentioned as requiring caution due to its potential to provoke seizures?
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Which of these symptoms is least likely to be directly associated with intoxication of sedative/hypnotics?
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Which of the following conditions is commonly managed alongside supportive care for sedative/hypnotic intoxication?
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What is the role of NAPQI in acetaminophen toxicity?
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Which treatment for acetaminophen overdose is preferred due to fewer side effects?
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Which of the following presentations indicates a potential severe liver damage after acetaminophen ingestion?
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What management strategy should be employed for hypotension caused by sympatholytic substances?
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In the context of heroin or opioid overdose, which factor makes standard naloxone administration potentially ineffective?
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Which of the following statements accurately describes the use of flumazenil in benzodiazepine overdose?
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What is the primary mechanism of action employed by chelation agents in the treatment of heavy metal toxicity?
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Which heavy metal is commonly associated with industrial solvents and can cause severe health effects upon exposure?
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Which benzodiazepine is specifically noted for not reliably appearing on all urine drug screens?
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What is a major contraindication for the use of flumazenil in treating benzodiazepine overdose?
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What is the primary mechanism through which cyanide disrupts cellular metabolism?
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Which treatment is effective in converting cyanide to a less toxic substance in the body?
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What is a potential effect of high doses of dihydropyridine calcium channel blockers?
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What is the initial treatment approach for severe hypotension due to cyanide poisoning?
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Which factor makes carboxyhemoglobin testing unreliable shortly after administering hydroxocobalamin?
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Quais sintomi sunt typicamente associati con avvelenamento da Digoxin?
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Qual es le mechanismos de action de Digoxin?
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In le casus de intossicazione da Digoxin, qual es le treatment appropriate?
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Qual es le treatment emergente pro hemorrhagia intracraniale in un paciente con anticoagulante?
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Qual es un effecto collaterale possibile de Digoxin?
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What are the potential consequences of acute ethylene glycol intoxication?
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Which treatment specifically inhibits the formation of toxic metabolites in methanol poisoning?
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What is a notable clinical feature of methanol intoxication during its intermediate phase?
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Which mechanism explains the action of sulfonylureas in the event of a hypoglycemic episode?
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Which of the following medications is NOT associated with the treatment of opioid overdose?
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What symptom is primarily associated with beta-blocker overdose?
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Which metabolic disorder is linked to ethylene glycol metabolism in the human body?
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In treating severe valproate overdose, which treatment is likely to be used?
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What is a common presentation of opioid overdose?
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What is the dosage strategy for glucagon in treating beta-blocker overdose?
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Study Notes
Toxicology and Epidemiology
- In 2017, there were over 2.12 million calls made to poison control centers concerning human exposures.
- More than half of these calls, exceeding 1 million, were related to incidents involving children.
- Highlights the significant concern for child safety and the risks associated with toxic exposures.
- Emphasizes the importance of poison control as a critical resource for addressing toxicology-related emergencies.
Epidemiology of Toxicology
- In 2017, poison control centers received over 2.12 million calls related to human exposure to toxins.
- Children accounted for more than 1 million of these calls, highlighting their vulnerability to poisoning incidents.
- Analyzing these statistics can inform preventative measures and education initiatives aimed at reducing accidental poisonings, especially among young populations.
Epidemiology of Toxicology
- In 2017, there were over 2.12 million calls made to poison control centers due to human exposures.
- Children accounted for more than 1 million calls, highlighting their vulnerability to poisoning incidents.
- The data underscores the importance of preventative measures and education regarding toxic substances, particularly in households with young children.
Cholinergic Substances
- Includes organophosphates, pesticides, sarin gas, and specific medications (e.g., Neostigmine, Edrophonium).
- Organophosphates are commonly found in agricultural pesticides and are associated with nerve agents.
Mechanism of Action
- Blocks acetylcholinesterase, preventing the breakdown of acetylcholine.
- Results in an accumulation of acetylcholine at the neuromuscular junction (NMJ).
- Causes a hypercholinergic response, leading to overstimulation of cholinergic receptors.
Clinical Presentation (SLUDGEM)
- Salivation: Excessive saliva production.
- Lacrimation: Increased tear production.
- Urination: Frequent urination.
- Defecation/Diarrhea: Increased bowel movements and gastrointestinal upset.
- GI Pain: Abdominal discomfort.
- Emesis: Nausea and vomiting.
- Miosis: Constriction of pupils, indicating overstimulation.
- Characterized by a "leaky" or wet presentation; fluids are secreted from multiple systems.
- Immediate life-threatening symptoms include bradycardia, bronchorrhea (excess lung secretions), and bronchospasm (tightening of airways).
Treatment Approaches
- Decontaminating: Essential to remove exposure to pesticide or nerve agent; formal decontamination procedures are required.
- Supportive Care: Key for managing adverse reactions and stabilizing the patient.
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Antidotes:
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Mark 1 Kit/Duo Dote:
- Contains a 2mg IM atropine autoinjector.
- Atropine works by competitively blocking muscarinic receptors and requires substantial ongoing dosing.
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2-PAM (Pralidoxime):
- Contains a 600mg IM autoinjector.
- Helps to bind to organophosphates and reactivates acetylcholinesterase (AchE) to restore normal function.
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Mark 1 Kit/Duo Dote:
- After initial symptoms are managed, continuous administration of antidotes is necessary for effective treatment.
Anticholinergics Overview
- Anticholinergics include substances like Atropine, which is found in Lomotil and can be misused for its narcotic effects.
- Antihistamines may be abused for their psychotic effects, while unintentional exposure can occur with various medications.
- Other classes related to anticholinergic effects include TCAs (tricyclic antidepressants), SSRIs (selective serotonin reuptake inhibitors), muscle relaxers (e.g., Cyclobenzaprine), anti-Parkinsonian medications, and certain herbals like Jimson Weed and Amanita Mushroom.
Mechanism of Action
- Anticholinergics work by competitively antagonizing (blocking) muscarinic receptors, primarily affecting peripheral nervous system activity.
- Central nervous system (CNS) effects may vary based on the specific substance involved.
Clinical Presentation
- Symptoms encompass a classic triad referred to as "Dry as a bone" indicating extreme dryness and anhidrosis (lack of sweating), even in elevated temperatures.
- Patients may experience "Hot as a hades" hyperthermia, which can deteriorate with increased agitation or restraint.
- Skin may present as "Red as a beet," reflecting cutaneous vasodilation and flushing.
- "Blind as a bat" refers to non-reactive mydriasis (dilated pupils), complicating visual responsiveness.
- "Mad as a hatter" describes possible acute delirium, lethargy, and hallucinations.
- "Full as a flask" characterizes acute urinary retention, which must be noted as not equivalent to typical urinary retention.
Substances
- Cocaine, amphetamines, methamphetamines, ecstasy (MDMA), synthetic cannabinoids, and bath salts are classified as sympathomimetics.
- A 2018 Department of Health warning highlighted risks associated with synthetic cannabinoids, specifically those adulterated with vitamin K antagonists leading to coagulopathy.
Mechanism
- Sympathomimetics increase sympathetic tone, having mixed effects on alpha and beta adrenergic receptors.
Presentation
- Symptoms typically indicate heightened physiological states:
- Hyperthermia
- Tachypnea
- Tachycardia
- Agitation and psychosis
- Mydriasis (dilated pupils)
- Increased motor activity (hypermotor)
- Excessive sweating (hyperhidrosis)
- Excited delirium is a major complication, often leading to significantly elevated health risks.
- Potential complications include:
- Acidosis
- Rhabdomyolysis, resulting in myoglobin clogging renal tubules
- Hyperkalemia, which can progress to irreversible ventricular fibrillation and death
Treatment
- Supportive care is crucial in managing symptoms and complications.
- First-line sedatives include benzodiazepines (BZDs).
- Consider nitroprusside for treating refractory hypertension.
- Paralyze and intubate if necessary, ensuring adequate airway management.
- Aggressive hydration is essential to prevent rhabdomyolysis and acute kidney injury (AKI).
- Phentolamine may be used for alpha-1 blockade but should be administered cautiously and only in refractory cases after toxicology consultation.
DONT’S
- Avoid using succinylcholine for intubation due to the risk of potassium shifts in patients who may already have hyperkalemia.
- Do not administer antipyretics as hyperthermia is not indicative of traditional fever; it is a critical symptom necessitating other interventions.
- Avoid pure beta-blockade due to the risk of unopposed alpha activity, which can complicate cardiac function, potentially leading to heart failure and pulmonary edema.
Sedative/Hypnotics Overview
- Includes various substances that depress the central nervous system (CNS), leading to sedation, hypnosis, or anxiolysis.
Substances
- Barbiturates: Older class of sedatives, often associated with higher overdose risk.
- Phenobarbital: Commonly used for seizure disorders; a barbiturate.
- Fioricet: Combination medication for migraines, containing acetaminophen, caffeine, and butalbital (a barbiturate).
- Benzodiazepines: Includes drugs like alprazolam and lorazepam; often used for anxiety and insomnia.
- Flunitrazepam (Rohypnol): Notorious for its use in cases of drug-assisted assault; potent benzodiazepine.
- Gamma Hydroxybutyrate (GHB): Central nervous system depressant with potential for misuse.
- Opioids: Includes natural and synthetic substances; watch for interaction with medications like lomotil and loperamide.
- Alcohols: Various types including ethanol (beverage alcohol), ethylene glycol (antifreeze), isopropyl (rubbing alcohol), and methanol (wood alcohol); all can be toxic.
Mechanism of Action
- Substance Dependence: Effects vary based on the specific substance used.
- GABA Binding: Most sedatives share a mechanism by binding to GABA receptors, enhancing inhibitory neurotransmission.
- Opioid Receptors: Opioids specifically bind to Mu, Kappa, and Delta receptors, influencing pain and reward pathways.
- CNS Depressant Effects: All mentioned substances contribute to CNS depression, affecting various bodily functions.
Clinical Presentation
- CNS Depressive Symptoms: Symptoms include slurred speech, nystagmus (involuntary eye movement), and ataxia.
- Opioid-Specific Signs: Miosis (pinpoint pupils) is a key indicator of opioid ingestion.
- Other Symptoms: Nausea/vomiting, respiratory depression, altered mental status (AMS).
- Severe Cases: Hypoglycemia and hypothermia may occur if individual is unresponsive for a prolonged period.
- Intoxication Spectrum: Severity of symptoms can range widely depending on the dosage and individual response.
Treatment
- Supportive Care: Critical for all cases; includes monitoring vital signs and ensuring patient safety.
- Airway Management: Immediate intervention required if the patient cannot protect their own airway.
- Respiratory Support: Oxygenation and ventilation assistance may be necessary.
- IV Hydration: Important for maintaining fluid balance and managing electrolyte disturbances.
- Electrolyte Correction: Treating imbalances is essential for stabilizing the patient.
- Substance-Specific Antidotes: Administer antidotes as needed for specific substances.
- Caution with Flumazenil: While it's an antidote for benzodiazepine overdose, it may provoke seizures in some patients.
- Disposition: Based on the specific substance involved and patient response to treatment.
Sympatholytic Agents: Clonidine
- Clonidine is classified as an imidazoline sympatholytic agent.
- Functions as an alpha-2 adrenergic and partial opioid receptor agonist.
- Clinical presentation resembles sedative-hypnotic effects but lacks typical response to Naloxone treatment.
- Management involves high-dose naloxone and infusions (gtts) to counteract symptoms.
- For hypotension, vasopressors are utilized due to alpha receptor effects.
- Bradycardia management may rely on atropine or the chronotropic effects of vasopressors.
Acetaminophen (APAP) Toxicity
- Acetaminophen metabolizes into N-acetyl-p-benzoquinone imine (NAPQI).
- NAPQI undergoes detoxification by glutathione in the liver until depletion occurs.
- Excess NAPQI leads to hepatocellular death and liver damage.
Clinical Presentation
- Early stages can be asymptomatic, leading to gradual progression toward liver failure.
- Immediate blood tests for APAP levels are critical, with follow-up at 4 hours.
Treatment and Antidote
- N-acetylcysteine (NAC) is the recommended antidote for acetaminophen toxicity.
- NAC can be administered either intravenously or orally; oral administration has fewer side effects.
- Risks associated with IV NAC include anaphylaxis, rash, urticaria, pruritus, flushing, nausea/vomiting, and bronchospasm.
Diagnosis of Acetaminophen Overdose
- Use of the Rumack-Matthew Nomogram to assess the likelihood of toxicity.
- Acetaminophen levels should be monitored in patients over 12 years who experienced a single, acute overdose within 4 to 24 hours post-ingestion.
- Severe liver damage is likely in 90% of cases with levels exceeding 300 mg/ml at 4 hours or 45 mg/ml at 15 hours post-ingestion.
- The nomogram also determines if antidote administration is necessary.
Additional Management
- Potentially severe side effects from NAC necessitate readiness for ancillary treatments, including antihistamines, steroids, beta-agonists, or epinephrine.
Benzodiazepines
- Mechanism involves enhancing GABA effects by binding to benzodiazepine (BZD) receptors.
- Presentation includes sedative/hypnotic effects leading to altered mental status (AMS) and respiratory depression.
- Treatment primarily consists of supportive care, with the option of Flumazenil, a competitive GABA antagonist, though its use is rare.
- Flumazenil can induce seizures if the patient has a history of seizures—recommended treatments include Phenobarbital or Diprivan.
- Contraindications for Flumazenil include:
- Chronic benzodiazepine use, which can worsen acute withdrawal symptoms.
- Suspected tricyclic antidepressant (TCA) overdose.
- Co-ingestion of seizure-inducing agents or stimulants.
- Known seizure disorders.
- Increased intracranial pressure.
- Certain benzodiazepines, such as Alprazolam, Lorazepam, and Clonazepam, may not be detected on all urine drug screens (UDS).
Heavy Metals
- Common heavy metal substances include arsenic, iron, lead, and mercury.
- Sources of heavy metals include wood preservatives, industrial solvents, elemental iron, medications, paint chips, fuels, and batteries.
- Presentation of toxicity symptoms varies significantly depending on the specific substance involved.
- Treatment for heavy metal poisoning is chelation therapy, utilizing specific agents for different toxins to bind and convert them into non-toxic compounds for elimination from the body, either through excretion or dialysis.
Calcium Channel Blockers
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Dihydropyridines cause hypotension and reflex tachycardia due to peripheral vasodilation.
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High doses of dihydropyridines can lead to loss of peripheral selectivity, resulting in bradycardia.
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Non-dihydropyridines primarily cause bradycardia and hypotension by decreasing heart rate (chronotropy) and heart muscle contraction strength (ionotropy).
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Treatment for Calcium Channel Blocker Overdose:
- Administer 3g IV of calcium gluconate.
- Infuse at a rate of 10-50 mg/kg/hr, titrated to blood pressure.
- Establish insulin infusion at 1 unit/kg/hr.
- Provide concomitant dextrose and potassium supplementation.
- Use intravenous fluid (IVF) and vasopressors to support blood pressure.
Cyanide Poisoning
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Sources of Cyanide Exposure:
- Burning of plastics or polymers, common in house fires.
- Chemical warfare and intentional poisoning scenarios.
- Prolonged infusion of nitroprusside for more than 48 hours.
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Mechanism of Cyanide Toxicity:
- Binds to cytochrome oxidase in mitochondria, disrupting electron transport.
- Shifts cellular metabolism from aerobic to anaerobic, leading to metabolic dysfunction.
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Presentation of Cyanide Poisoning:
- Early Symptoms: Headache, confusion, tachycardia, hypotension, and tachypnea.
- Late Symptoms: Nausea and vomiting, bradycardia, potential arrhythmias, asystole, and altered mental status (AMS).
- Narrow difference between arterial and venous partial pressure of O2; crucial in assessing enclosed fire victims due to potential carbon monoxide exposure.
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Treatment for Cyanide Poisoning:
- Administer hydroxocobalamin at 70 mg/kg IV over 15 minutes, with a maximum dose of 5g; acts as a direct binder to cyanide for renal excretion.
- Colorimetric testing may be ineffective for 72 hours post-administration; manual CBC required as SP02 and carboxyhemoglobin assessments may be unreliable.
- Sodium thiosulfate given at 1.65 ml/kg IV over 10 minutes; converts cyanide into less toxic thiocyanate.
- Sodium bicarbonate used to correct acidosis and enhance the efficacy of sodium thiosulfate.
Digoxin Overview
- Digoxin inhibits the sodium/potassium pump in myocardial cells, increasing intracellular calcium, which enhances cardiac contractility.
Presentation of Digoxin Toxicity
- ECG Changes: Can include various arrhythmias, often characterized by characteristic ST segment changes.
- Bradycardia: Resulting from increased vagal tone, potentially leading to significant heart rate reduction.
- Neurological Symptoms: Confusion and delirium may occur in cases of toxicity, indicating central nervous system effects.
- Visual Disturbances: Patients may experience yellow halos around lights or scotomas, suggesting altered vision.
- Electrolyte Disarray: Changes in electrolytes, especially potassium levels, are commonly seen and can exacerbate toxicity.
Treatment for Digoxin Toxicity
- Digoxin Immune Fab (Digibind): Administered based on serum levels and presenting symptoms; effective in reversing digoxin effects.
Anticoagulant Management
- Heparin/LMWH: Used for anticoagulation; protamine can be administered (25-50 mg over 10 minutes) to reverse effects if needed.
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Warfarin:
- Emergent Situations (e.g., intracranial hemorrhage): Require immediate reversal with prothrombin complex concentrate, IV Vitamin K, and fresh frozen plasma (FFP).
- Non-Emergent Situations (INR >9): Can use IV/oral Vitamin K and may consider FFP.
- NOACs (Novel Oral Anticoagulants): Prothrombin complex concentrate can also be used for reversal in cases of significant bleeding or overdose.
Alcohols
- Ethylene Glycol: Used in anti-freeze, brake fluid, hydraulic fluids, and solvents.
- Methanol: Commonly found in windshield washer fluid and various solvents.
Mechanisms of Toxicity
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Ethylene Glycol:
- Initially causes CNS depression.
- Results in elevated osmolar gap.
- Metabolizes into oxalic acid and glycolic acid, leading to metabolic acidosis.
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Methanol:
- Converted to formaldehyde via alcohol dehydrogenase.
- Eventually metabolizes to formic acid, which causes downstream lactic acidosis, albeit very slowly.
Presentation of Intoxication
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Ethylene Glycol:
- Early signs of intoxication may include CNS effects.
- Intermediate phase (12-24 hours) shows hypertension, tachypnea, and hypocalcemia.
- Late phase features renal failure.
- Notable characteristic: fluoresces under Wood’s lamp.
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Methanol:
- Symptoms include confusion, ataxia, altered mental status, seizures, and visual disturbances.
- Tachypnea due to anion gap acidosis.
- Symptoms manifest 12-24 hours after exposure.
Treatment Options
-
General Treatment for Both:
- Fomepizole (15 mg/kg loading dose) inhibits alcohol dehydrogenase, preventing toxic metabolite formation.
-
Beta Blockers:
- Mechanism: Non-selective or selective beta-1 adrenergic receptor antagonism.
- Symptoms include bradycardia, hypotension, delirium, seizures (notably from propranolol), hypothermia, and hypoglycemia.
- Treatment involves glucagon (5 mg IVP), calcium gluconate (3 g IV), and insulin (1 unit/kg/hr) with concurrent dextrose and potassium supplementation for hypoglycemia.
Sulfonylureas
- Mechanism: Stimulates insulin release from pancreatic beta-cells.
- Presentation: Persistent hypoglycemia and related sequelae.
- Treatment: Dextrose 50% for acute hypoglycemia, D10/0.45% NaCl titrated to achieve euglycemia, and octreotide to slow insulin release.
Valproate
- Mechanism: Enhances GABA effects through competitive agonism.
- Presentation: CNS depression, hypotension, and respiratory depression.
- Treatment: Naloxone for potential non-selective opioid effects, levo-carnitine (100 mg/kg loading dose), and dialysis for severe cases.
Opioids
- Mechanism: Competitive agonists of opioid receptors.
- Presentation: CNS depression, respiratory depression, and miosis.
- Treatment: NARCAN (initial dose 0.4 mg-2 mg IVP), with further doses if necessary, to achieve a GCS of 13-14. Care must be taken to avoid rapid withdrawal due to aggressive dosing.
General Workup
- Conduct a thorough history and physical examination for accurate assessment.
- Utilize ECG for arrhythmias, blocks, and QTc abnormalities.
- Lab tests may include POC glucose, CBC, CMP, magnesium, CK, lactic acid, ethanol, specific drug levels, and a pregnancy test.
- Provide supportive care during evaluation until antidotes or metabolic assistance is available. Consider contacting poison control as necessary.
One Pill Kill
- Some medications can be fatal to children in small doses: clonidine, quinine, suboxone, calcium channel blockers, sulfonylureas, and tricyclic antidepressants.
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Description
This quiz covers key aspects of toxicology, including statistics on poison control calls, particularly focusing on child exposures. It highlights the significance of understanding toxicological data and its implications for public health. Test your knowledge on the epidemiology related to toxic substances.
