143 General Approach to the Poisoned Patient
Key Points• The mainstay of treatment of a poisoned patient is good symptomatic and supportive care.
• Observation is one of the most critical aspects in the management of poisoned patients.
• The most common substance categories associated with fatalities are sedative-hypnotics, antipsychotics, cardiovascular medications, opioids, and acetaminophen combination products.
• All substances can be poisonous; toxicity usually depends on the dose and the duration of exposure.
• Toxidromes are symptom complexes that may provide clues to the identity of the offending agent on the basis of specific pharmacologic principles; they represent “physiologic fingerprints.”
• In general, hypotension in the setting of poisoning is best treated with direct-acting pressors.
• In patients with an unknown ingestion, activated charcoal is the most efficacious decontamination method, but its use should be limited to those who are awake and alert and/or have a protected airway (self-protected or intubated).
Epidemiology
It is believed that approximately 5.3 million poisoning exposures take place every year in the United States, but only about half are reported to poison control centers. The American Association of Poison Control Centers reported 2,479,355 cases of poisoning during 2009, with 93.8% occurring at a residence and just 1.5% at the workplace. Children younger than 3 years were involved in 46.0% of reported poisonings. About 82% of the poisonings were unintentional, and suicide attempts accounted for just 8.9% of cases.1
Presenting Signs and Symptoms
A poisoned patient may have many different clinical symptoms, including cardiac dysrhythmias, altered mental status, seizures, nausea and vomiting, and respiratory depression. In many cases the offending agent is initially unknown. Vital signs, including pulse oximetry values, are important to obtain (Table 143.1) and should be measured often in a poisoned patient. Vital signs (temperature, pulse, respirations, blood pressure, pulse oximetry) are helpful because they can provide clues to the type of poisoning. Physical findings such as pupil size, odor, seizure activity, and dermatologic changes can also provide clues to the offending agent (Tables 143.2 to 143.4). Emergency physicians (EPs) should be sure to examine for diaphoresis under the axilla, which may be the only body part that exhibits this finding. It is essential to note that patients with mixed ingestions may not have the classic initial signs and symptoms.
Table 143.1 Classic Examples of Ingested Substances Associated with Changes in Vital Signs*
| CHANGE IN VITAL SIGN | ASSOCIATED SUBSTANCES |
|---|---|
| Bradycardia | |
| Tachycardia | |
| Hypothermia | |
| Hyperthermia | |
| Hypotension | |
| Hypertension | |
| Hypoventilation | |
| Hyperventilation |
* This is not an all-inclusive list. Victims of multiple substance exposure often do not have the classic signs and symptoms.
Table 143.2 Specific Substances Associated with Pupillary Changes*
| PUPILLARY CHANGE | ASSOCIATED SUBSTANCES |
|---|---|
| Miosis | |
| Mydriasis |
* Patients with mixed ingestions often do not have the classic pupillary changes.
Table 143.3 Specific Substances Associated with Skin Changes
| SKIN CHANGE | ASSOCIATED SUBSTANCES |
|---|---|
| Diaphoresis | |
| Red skin | |
| Blue skin | Methemoglobin-forming agents (e.g., nitrates, nitrites, aniline dyes, dapsone, phenazopyridine) |
| Blisters |
Table 143.4 Specific Substances Associated with Odors
| ODOR | ASSOCIATED SUBSTANCE |
|---|---|
| Bitter almonds | Cyanide |
| Carrots | Water hemlock |
| Fruity | Ketones (from diabetic ketoacidosis), isopropanol (metabolized to acetone) |
| Garlic | Arsenic, organophosphates |
| Gasoline | Hydrocarbons |
| Mothballs | Camphor |
| Peanuts | Certain rodenticides |
| Pears | Chloral hydrate |
| Rotten eggs | Hydrogen sulfide, sulfur dioxide |
| Wintergreen | Methyl salicylates |
The history obtained from the patient may be unreliable.2 It is crucial for emergency department (ED) personnel to also obtain additional history from family and friends. The paramedics who brought the patient can provide information about the scene where the overdose took place. What behavior did the patient have at the scene or before arrival? Were there seizures, emesis, changing vital signs? Were there any medicine bottles were found and, if so, were any pills were missing from the bottles? The patient’s primary care physician or psychiatrist may provide important information. Frequently, the patient’s pharmacy can be called to obtain lists of current medications and the last fill date. It is crucial to obtain an occupational history and to review past medical records for any poisoned patient. The initial work-up should determine whether a specific patient has been exposed to an agent for which an antidote (or other specific treatment) exists (Box 143.1).
Differential Diagnosis and Medical Decision Making
Toxidromes
Several drugs and toxins are associated with specific toxidromes (Table 143.5). Toxidromes are symptom complexes that may provide clues to the identity of the offending agent. They are based on specific pharmacologic principles and represent the “physiologic fingerprints” of the associated substances. An anticholinergic toxidrome, for example, is caused by parasympatholytic substances such as antihistamines, jimsonweed, tricyclic antidepressants (TCAs), and phenothiazines. Affected patients may exhibit hypertension, tachycardia, fever, delirium, and mydriasis. Sympathomimetic toxidromes resemble anticholinergic toxidromes except that parasympatholytic agents produce silent bowel sounds and dry skin.
Table 143.5 Toxidromes and Their Causes
| TOXIDROME | FEATURES | EXAMPLES OF CAUSES* |
|---|---|---|
| Anticholinergic: “Hot as a hare, dry as a bone, red as a beet, blind as a bat, mad as a hatter, full as a flask, tachy as a pink flamingo” | ||
| Cholinergic: “SLUDGE syndrome and killer BBBs”† | ||
| Extrapyramidal | ||
| Opioid | ||
| Sedative-hypnotic | ||
| Serotonin | ||
| Sympathomimetic | ||
| Delayed | Patients may not have any initial symptoms |
CNS, Central nervous system; GI, gastrointestinal; LSD, lysergic acid diethylamide; MAOIs, monoamine oxidase inhibitors.
* This is by no means a comprehensive listing of causes of toxidromes.
† Killer BBBs are the true life threats of this toxidrome and indicate very severe poisoning.
‡ Meperidine dilates the pupils; propoxyphene and pentazocine may not cause miosis.
§ With transdermal patch–released medications, toxidromes may have a slower onset.
The following diagnostic studies should be performed in poisoned patients: serum acetaminophen and acetylsalicylic acid measurements, blood ethanol measurement, blood chemistry panel, electrocardiogram (ECG), pulse oximetry, and serum glucose measurement (Box 143.2). Toxicology screening may confirm exposure to a toxicant but does not usually change management (see later discussion). A blood chemistry profile can be extremely useful, especially in determining the anion gap.3,4 The anion gap is calculated by the formula (mEq/L) + Na+ − [Cl− + HCO3− ]; the normal range of anion gap varies from 3 to 12 mEq/L. An increase in the anion gap may indicate an intoxication, but EP must be aware that a normal anion gap does not rule out poisoning. Conditions such as hypoalbuminemia can alter the anion gap. Every 1-g/L decrease in plasma albumin leads in a drop in the anion gap of 2.5 mEq/L. Multiple conditions can cause metabolic acidosis with an elevated anion gap, and the mnemonic “A CAT MUD PILES” is an easy way to remember most of them (Box 143.3). It is important to note than any toxin that can cause seizures or other processes leading to lactic acidosis can also cause an anion gap. A decreased anion gap can be seen with bromide and lithium poisonings.
