General Approach to the Poisoned Patient

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143 General Approach to the Poisoned Patient

Acknowledgment and thanks to Victor Tuckler, MD, and Jorge Martinez, MD, for their work on the first edition.

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

Patients who have ingested poisons may not appear to be critically ill initially, but they all have the potential for clinical deterioration.

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.