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Toxicology – APPROACH TO THE POISONED PATIENT
ABC’s:
As with all emergency department patients, first ensure the patient has a patent airway, is breathing, and has a pulse. Immediate intervention is required if any or all of these are absent.
Vital Signs:
Temperature, heart rate, blood pressure, respiratory rate, and O₂ saturation will help guide the diagnosis and help categorize the intoxication or overdose into one of the more common toxidromes.
History:
Attempt to get a good history using collateral sources if possible, as the poisoned patient is often unreliable or containers altered. EMS, family members, occupation, past medical records, and empty pill bottles can provide insight into the potential toxin or overdose.
Physical:
In addition to vital signs, physical examination will help tease out the clinical toxidrome.
PEARLS
ABC’s:
As with all emergency department patients, first ensure the patient has a patent airway, is breathing, and has a pulse. Immediate intervention is required if any or all of these are absent.
Vital Signs:
Temperature, heart rate, blood pressure, respiratory rate, and O₂ saturation will help guide the diagnosis and help categorize the intoxication or overdose into one of the more common toxidromes.
History:
Attempt to get a good history using collateral sources if possible, as the poisoned patient is often unreliable or containers altered. EMS, family members, occupation, past medical records, and empty pill bottles can provide insight into the potential toxin or overdose.
- What: Consider what medications the patient has access to including his or her own, as well as those of parents, friends, significant others, children and visiting relatives. Ask if the drug is an immediate-release or sustained-release product.
- When: A time frame of suspected ingestion can influence treatment options and patient disposition. For example, some toxins have a delayed onset and some antidotes must be given within a specific time frame.
- Dose: Assume that any unreliable patient took the highest possible dose. Count the number of pills remaining in their prescription bottles and subtract that amount from the initial number prescribed. Assume all missing pills were taken as a single overdose.
- Why: Was this an accidental ingestion, a therapeutic misadventure in pursuit of a “high” or in pursuit of better treatment outcomes, or was it a suicide attempt? The answer will help determine the patient’s disposition.
- Coingestions: Multiple drug ingestions are common; alcohol is the most common coingestion.
Physical:
In addition to vital signs, physical examination will help tease out the clinical toxidrome.
- Mental Status: Agitation / somnolence / paranoid / obtunded / comatose
- Skin: Wet / dry / cyanotic / erythematous / pale / hot / cold
- Eyes: Miosis / mydriasis / nystagmus / conjunctival injection / jaundice
- Mucous Membranes: Wet and salivating / dry and chapped
- Heart/EKG: Tachycardia / bradycardia / QRS widened / QT prolongation
- Lungs: Tachypnea / bradypnea / rales / wheezing / crackles
- Bowel Sounds: Hyperactive / normal / absent
- Neurological: Hyperreflexia / hyporeflexia
PEARLS
- US Poison Control Center: 1-800-222-1222
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Toxicology – Drugs Causing Hyperventilation
Aspirin (Salicylates)
Salicylates directly stimulate the respiratory center in the central nervous system, leading to increased respiratory rate and the development of respiratory alkalosis.
Amphetamines (Speed)
Amphetamines and other sympathomimetic agents elevate catecholamine levels, resulting in increased heart rate, blood pressure, and respiratory rate, often causing hyperventilation.
Paraquat
Paraquat, a toxic herbicide, causes direct lung injury leading to impaired oxygen exchange. This results in hypoxia and compensatory hyperventilation.
Phencyclidine (PCP)
PCP is a dissociative anesthetic that produces minimal cardiopulmonary depression. Patients may fluctuate between sedation and agitation, with hyperventilation commonly occurring during agitated states.
Noncardiogenic Pulmonary Edema (NCPE)
Various toxins can lead to noncardiogenic pulmonary edema, impairing gas exchange and triggering hyperventilation. Inhaled causes include ammonia, chlorine gas, solvents, hydrocarbons, hydrogen sulfide, and phosgene. Oral or parenteral agents include heroin, methadone, naloxone, salicylates, NSAIDs, and certain chemotherapeutic drugs.
Toxin-Induced Metabolic Acidosis
Certain toxins produce metabolic acidosis, which stimulates compensatory hyperventilation (hyperpnea) as the body attempts to reduce carbon dioxide levels and correct acidemia.
Aspirin (Salicylates)
Salicylates directly stimulate the respiratory center in the central nervous system, leading to increased respiratory rate and the development of respiratory alkalosis.
Amphetamines (Speed)
Amphetamines and other sympathomimetic agents elevate catecholamine levels, resulting in increased heart rate, blood pressure, and respiratory rate, often causing hyperventilation.
Paraquat
Paraquat, a toxic herbicide, causes direct lung injury leading to impaired oxygen exchange. This results in hypoxia and compensatory hyperventilation.
Phencyclidine (PCP)
PCP is a dissociative anesthetic that produces minimal cardiopulmonary depression. Patients may fluctuate between sedation and agitation, with hyperventilation commonly occurring during agitated states.
Noncardiogenic Pulmonary Edema (NCPE)
Various toxins can lead to noncardiogenic pulmonary edema, impairing gas exchange and triggering hyperventilation. Inhaled causes include ammonia, chlorine gas, solvents, hydrocarbons, hydrogen sulfide, and phosgene. Oral or parenteral agents include heroin, methadone, naloxone, salicylates, NSAIDs, and certain chemotherapeutic drugs.
Toxin-Induced Metabolic Acidosis
Certain toxins produce metabolic acidosis, which stimulates compensatory hyperventilation (hyperpnea) as the body attempts to reduce carbon dioxide levels and correct acidemia.
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