the pharmacokinetic features of the toxin ( eg, circulating

half-life) can be markedly prolonged secondary to

extended absorption times and the saturation of metabolizing enzymes. These toxicokinetic principles often result

in an unpredictable onset of symptoms and overall duration of toxicity.

The initial goal in managing a poisoned patient is to

provide excellent supportive care. Contact your regional

poison center ( 1 -800-222-1222) early in the management of your patient as they can provide invaluable

support. To aid in making the diagnosis, attempt to classify the patient's clinical presentation into a specific

toxidrome (a syndrome complex that characterizes

• Always focus on supportive measures first in the clin ical

management of poisoned patients.

• Consult your regional poison center (1-800-222-1 222)

to ensure the appropriate management of poisoned

patients.

certain classes of poisonings) (Table 54- 1). Only by following the preceding guidelines will certain patients be

suitable for decontamination measures and possibly

focused antidotal care.

CLINICAL PRESENTATION

� History

When possible, obtain a thorough history, including the

location of the exposure and the patient's occupation.

Pill bottles found at the scene or chemical containers

noted by emergency medical service, family, or friends

may provide the necessary clues to identify the causative

toxin. Attempt to establish the exact time of exposure,

although this is often limited to when the patient was

last seen in a "normal" condition. Try to discern the

amount that was ingested and whether it was in a regular or extended release formulation. Finally, try to establish the chronicity of the exposure, the immediate

symptoms after the exposure, a history of previous suicide attempts, a thorough past medical history, and a

history of any illicit drug abuse. If known, contacting

the patient's regular pharmacy may provide further

insight into the case.

230

THE POISONED PATIENT

Table 54-1. Common toxidromes.

Representative Additional Signs/

Toxidrome agent(s) Most Common Findings Symptoms Potential Interventions

Opioid Heroin, morphine CNS depression, miosis, respiratory Hypothermia, bradycardia, Ventilation or naloxone

depression respiratory arrest,

acute lung injury

Sympathomimetic Cocaine, amphetamine Psychomotor agitation, mydriasis, Seizures, rhabdomyolysis, Cooling, sedation with

diaphoresis, tachycardia, myocardial infarction, benzodiazepine, hydration

hypertension, hyperthermia cardiac arrest

Cholinergic Organophosphate Sal ivation, lacrimation, diaphoresis, Bradycardia, seizures, Airway protection and

insecticides, nausea, vomiting, urination, respiratory failure ventilation, atropine,

carbamate defecation, muscle fascicula- pralidoxime

insecticides tions, weakness, bronchorrhea

Anticholinergic Scopolamine, atropine AMS, mydriasis, dry /flushed skin, Seizures, dysrhythmias, Physostigmine (if applicable),

urinary retention, decreased rhabdomyolysis sedation with benzodiazepine,

bowel sounds, hyperthermia, cooling, supportive

dry mucous membranes management

Salicylates Aspirin, oil of AMS, respiratory alkalosis, Low-grade fever, MDAC, alkalinization of the urine

wintergreen metabolic acidosis, tinnitus, ketonuria, acute with K+ repletion, hemodialysis,

hyperpnea, tachycardia, lung injury hydration

diaphoresis, nausea, vomiting

Hypoglycemia Sulfonylureas, insulin AMS, diaphoresis, tachycardia, Paralysis, slurring of Glucose, octreotide

hypertension speech, seizures

Serotonin syndrome Meperidine or dextro- AMS, increased muscle tone, Intermittent whole-body Cooling, sedation with

methorphan and hyperreflexia, hyperthermia tremor benzodiazepine, supportive

MAOI; SSRI and TCA; management

SSRI/TCA/MAOI and

amphetamines; SSRI

alone

AMS, a ltered mental status; CNS, central nervous syndrome; MAOI, monoamine oxidase inhibitor; MDAC, m u lti-dose activated charcoal;

SSRI, seroton in reu ptake inhibitor; TCA, tricyclic antidepressant.

...,._ Physical Examination

Examination findings are very important to help recognize

potential toxidromes and identify to what class of agent

the patient might have been exposed. Obtain a full set of

vital signs to evaluate for evidence of hyperpyrexia,

hemodynamic instability, and tachypnea/hyperpnea (which

could indicate compensation for significant acidemia).

Characterize the patient's mental status and note any

neurologic deficits. Findings such as delirium, central

Table 54-2. Agents that affect pupil size.

Miosis (COPS)

Cholinergics, clonidine

Opioids, organophosphates

Phenothiazine, pilocarpine

Sedative-hypnotics

Mydriasis (AAAS)

Antihistamines

Antidepressants

Atropine (anticholinergics)

Sympathomimetics

nervous system ( CNS) hyperactivity, or frank obtundation/

coma may help to determine the responsible toxin. Perform

a careful ocular exam focusing on pupillary size and

responsiveness, the presence of nystagmus, and evidence of

abnormal lacrimation (Table 54-2). Finally, noting the

absence or presence of bowel sounds and whether the skin

is dry or wet may help differentiate anticholinergic from

sympathomimetic poisoning, respectively.

DIAGNOSTIC STUDIES

...,._ Laboratory

Obtain a basic metabolic panel looking for electrolyte

abnormalities or evidence of renal insufficiency. Check a

serum creatine phosphokinase in all patients with ongoing

seizures, prolonged down times, or renal abnormalities, as

rhabdomyolysis is a serious concern. Calculation of an

anion gap coupled to venous or arterial blood gas analysis

may help differentiate acid-base disorders. Co-oximetry

with blood gas analysis is also useful to determine

CHAPTER 54

methemoglobin and carboxyhemoglobin concentrations.

A markedly elevated serum lactate level (>8-10 mmol/L)

often indicates serious toxicity from an inhibitor of cellular

metabolism (eg, cyanide).

Quantitative blood screens for determining the serum

concentrations of multiple potential toxins including

acetaminophen, salicylates, lithium, carbamazepine,

valproic acid, lead, iron, and digoxin are usually very

helpful to guide the management of poisoned patients.

That said, qualitative urine toxicology screening rarely

changes the work-up, management, or disposition of emergency department patients. The frequent false-positive

results ( eg, positive for PCP due to dextromethorphan use)

and tests that remain persistently positive for several days

after the actual exposure ( eg, positive opiates x 7 days after

heroin use; positive cocaine x 3 days after cocaine use;

positive cannabinoids x 30 days after marijuana use) render urine toxicology screens challenging to interpret.

� Electrocardiogram

Obtain an electrocardiogram looking for any evidence of

dysrhythmias, conduction blocks, or abnormal intervals.

These findings may assist in both the diagnosis and treatment of patients poisoned by cardiotoxic agents.

� Imaging

Obtain computed tomography imaging of the brain when

either mental status changes or neurologic deficits are

present that are not consistent with the type of poisoning

being entertained (eg, focal or lateralizing signs). Order a

chest x-ray for all patients complaining of either shortness

of breath, hypoxia, toxic fume inhalation, or potential aspiration (eg, hydrocarbon ingestion). Check abdominal

x-rays,