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Toxidromes are constellations of signs and symptoms based primarily on vital signs and neuropsychiatric functions that are characteristic manifestations of certain toxic exposures. Recognition of the presence of a toxidrome can suggest a potential intoxicant and guide early interventions and management strategies. Examples of toxidromes include sympathomimetic, antimuscarinic, cholinergic, sedative-hypnotic, and opioid categories.
Qualitative urine drug assays have limited roles in the clinical setting and are inferior to quantitative serum levels in terms of guiding specific therapy.
Syrup of ipecac is not indicated in the emergency department (ED) care of a poisoned patient. Gastric lavage is not part of routine care. When given in a timely fashion (1-hour post ingestion), activated charcoal may be indicated for potentially lethal agents in alert, cooperative patients as noted in Figure 135.1 . Whole-bowel irrigation is rarely useful for management of poisoned patients but is potentially helpful for specific poisonings, such as metals, illicit drug packets, or sustained-release medications.
Serum alkalinization enhances urinary drug elimination for certain drugs and is indicated for significant poisoning caused by salicylates, phenobarbital, and methotrexate.
Hemodialysis is best suited to remove poisons of low molecular weight, low protein binding, and high water solubility; examples include methanol, ethylene glycol, lithium, and salicylates.
Regional Poison Control Centers (US: 1-800-222-1222) or a medical toxicologist can assist with antidotal therapy and may help facilitate patient disposition.
If the motivation behind the toxic exposure was self-harm, a psychiatric consultation is warranted. Patients with substance use disorders should be referred to a detoxification center or designated program.
Most poisoned patients seen in the emergency department (ED) are adults with intentional drug overdoses. The second most common scenario involves accidental poisoning in children, which actually represents the majority of calls to regional poison control centers. Additionally, other frequent causes of toxicity include: illicit drugs of abuse, accidental poisoning from pharmaceutical agents (drug-drug interactions as well as chronic toxicity), environmental exposures, and envenomations. Occupational chemical exposures, both industrial and agricultural, represent other important sources of potential toxicity. In the ED, it is important to evaluate and recognize scenarios where there may be immediate or delayed toxicity, in order to guide strategies for decontamination, enhanced drug elimination, and administration of antidotes when indicated.
When evaluating a patient with a particular ingestion, essential historical points include: the agent itself, the route of exposure, the amount ingested, possible co-ingestants, and the timing of the exposure. Knowing these facts can help make a determination regarding the expected course of care in the ED and help to mobilize diagnostic and therapeutic resources.
Oftentimes, the poisoned patient may be altered, obtunded, or uncooperative with the examiner. This leaves the history limited to that which can be gleaned from witnesses, such as paramedics or family, and the information generated from physical examination findings over which the patient does not have conscious control.
Historical information should be pulled from all available sources. A family member or friend may offer insight into the circumstances behind the patient’s exposure (e.g., intentional or accidental). Information regarding what medications or substances were available to the patient, and the timing of ingestion also is important. Paramedics should bring in all medication bottles present at the scene, not just the patient’s prescribed medications or alleged ingestion; if they do not, someone should be sent to the patient’s dwelling to retrieve them. Frequently, confusion as to what exactly was ingested can occur (e.g., ibuprofen mistaken for aspirin or acetaminophen) and this can lead a provider down the wrong path. A patient attempting suicide may intentionally mislead the ED staff, or medications may have been stored in mislabeled containers. Other sources of potentially useful information include state controlled-substance registries, pharmacy records, and previous medical records. Accessing the patient’s text-messaging history also may be helpful, if the patient consents to this or if friends and family provide this collateral information of their own accord.
For chemical exposures in either the home or workplace, avoid exposure to other individuals in the ED. Proper identification of the substance is important to initiate care and obtain product safety information, such as a Material Safety Data Sheet. Consequently, one could consider taking a picture of the label including any precise chemical numbers; if a substance is brought to the ED, take appropriate steps to avoid further exposure, such as sealing in an airtight container.
Poisoned patients are frequently unwilling or unable to participate in an interactive physical examination. The toxicologic physical examination, therefore, rests upon observing factors that do not require cooperation to elicit. Many ingested substances can cause derangement of the pulse, respiratory rate, as well as blood pressure. Rapid and accurate recording of the patient’s vital signs, including pulse oximetry and a rectal core temperature, should be done and repeated at appropriate intervals depending on the suspected toxin. Patients with hemodynamic instability or obtundation should be considered for continuous monitoring, at least initially until stabilized. The overall level of consciousness, pupillary size, and presence or absence of seizure activity may suggest a particular agent ( Boxes 135.1 and 135.2 ). Examination of the skin and mucous membranes with particular attention to discoloration and level of moisture may suggest poisoning by any of several agents ( Box 135.3 ); it may also reveal evidence of injection drug abuse, such as “track marks” or ulcerations from “skin popping.” A careful neurologic examination focusing on the level of muscle tone, clonus, or hyperreflexia can assist in the diagnosis of serotonin syndrome or neuroleptic malignant syndrome (NMS). Certain intoxicants may have particular odors associated with them; the presence of such an odor ought to alert the clinician to the possibility of poisoning by one of these agents ( Table 135.1 ); however, the absence of a characteristic smell does not exclude it.
L ead, lithium
E thanol, ethylene glycol, ethchlorvynol
T ricyclic antidepressants, thallium, toluene
H eroin, hemlock, hepatic encephalopathy, heavy metals, hydrogen sulfide, hypoglycemics
A rsenic, antidepressants, anticonvulsants, antipsychotics, antihistamines
R ohypnol (sedative hypnotics), risperidone
G amma-hydroxybutyrate (GHB)
I soniazid, insulin
C arbon monoxide, cyanide, clonidine
O rganophosphates, oral hypoglycemics
T ricyclic antidepressants
I soniazid, insulin
S ympathomimetics, strychnine, salicylates
C amphor, cocaine, carbon monoxide, cyanide, chlorinated hydrocarbons
A mphetamines, anticholinergics
M ethylxanthines (theophylline, caffeine), methanol
P hencyclidine (PCP), propranolol
B enzodiazepine withdrawal, botanicals (water hemlock, nicotine), bupropion, GHB
E thanol withdrawal, ethylene glycol
L ithium, lidocaine
L ead, lindane
S ympathomimetics
O rganophosphates
A cetylsalicylic acid or other salicylates
P hencyclidine (PCP)
Antihistamines, anticholinergics
Barbiturates and other sedative-hypnotics
Mustard gas
Snakes and spiders
Anticholinergics, niacin
Boric acid
Carbon monoxide (in morbid states)
Cyanide (rare)
Ergotamine
Nitrates
Nitrites
Aniline dyes
Phenazopyridine
Dapsone
Agent causing hypoxemia, hypotension, or methemoglobinemia
Bromides
Chlorinated aromatic hydrocarbons
Odor | Possible Source |
---|---|
Bitter almonds | Cyanide |
Carrots | Cicutoxin (water hemlock) |
Fruity | Diabetic ketoacidosis, isopropanol |
Garlic | Organophosphates, arsenic, dimethyl sulfoxide (DMSO), selenium |
Gasoline | Petroleum distillates |
Mothballs | Naphthalene, camphor |
Pears | Chloral hydrate |
Pungent aromatic | Ethchlorvynol |
Oil of wintergreen | Methylsalicylate |
Rotten eggs | Sulfur dioxide, hydrogen sulfide |
Freshly mowed hay | Phosgene |
Toxidromes are constellations of signs and symptoms based on autonomic and neurochemical processes that can suggest a particular class of exposure and direct management and therapy. The five traditionally described entities include the sympathomimetic, anticholinergic (antimuscarinic), cholinergic, sedative/hypnotic, and opioid toxidromes. In addition, withdrawal disorders, serotonin syndrome, and NMS have been well described.
This toxidrome is defined by a state of sympathomimetic excess, typically causing those effects expected from the “fight or flight” reaction. Patients are often in an altered state and may be delusional—especially with ingestion of substituted amphetamines, such as N -methyl-3,4-methylenedioxyamphetamine (MDMA: “ecstasy” or “molly”) or synthetic cannabinoids. Patients typically present with hypertension, tachycardia, and tachypnea. They may also be hyperthermic as a consequence of an increased metabolic rate. Mydriasis and diaphoresis may also be present. In severe overdoses, derangement of cardiac output can occur. Decreased diastolic filling time coupled with dysrhythmogenesis can result in circulatory collapse and shock, which may be refractory to fluid resuscitation and pressor agents.
The anticholinergic toxidrome is frequently encountered, because many pharmaceuticals have antimuscarinic properties. It manifests as a consequence of blocking normal cholinergic tone, causing an alteration in the normal homeostatic balance between the sympathetic and parasympathetic arms of the autonomic nervous system. This allows the sympathetic side to function unopposed and generates a state of relative sympathomimesis. Therefore, many of the symptoms attributable to the anticholinergic toxidrome—delirium, hyperthermia, mydriasis, and cutaneous flushing—share similarity with the sympathomimetic toxidrome. In contrast, because the secretory glands of the skin and mucous membranes contain muscarinic acetylcholine receptors, these patients are typically dry and not diaphoretic as found in the sympathomimetic toxidrome. The typical signs and symptoms can be recalled by the mnemonic “mad as a hatter, hot as a hare, blind as a bat, red as a beet, and dry as a bone.” Patients with severe anticholinergic toxicity are often altered and may be delusional, often requiring sedation in the emergency department (see Management section).
The cholinergic toxidrome results from overstimulation of the parasympathetic portion of the autonomic nervous system, which maintains the “rest and digest” functions. These patients typically have “fluids coming from every orifice” as a consequence of increased glandular secretion, and present with diaphoresis, urination, miosis, bronchorrhea, emesis, lacrimation, lethargy, and salivation ( Box 135.4 ). Agents of concern are primarily anticholinesterase agents, such as organophosphates and carbamate insecticides. These substances are readily available as pesticides; but they have also been engineered as weapons of mass destruction, typically referred to as nerve gases (e.g., sarin gas) and more recently the novel or Novichok agents. It is important to rapidly recognize this toxidrome because patients frequently die from excessive bronchorrhea, effectively drowning in their own secretions, unless timely antidotal therapy and cholinesterase regenerators are given.
D iarrhea, diaphoresis
U rination
M iosis
B radycardia
B ronchorrhea
E mesis
L acrimation
L ethargic
S alivation
M ydriasis
T achycardia
W eakness
T remors
F asciculations
S eizures
S omnolence
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