looking for radio-opaque ingestions (eg, leaded

paint chips or toys, batteries, selected drug packets) as

indicated to help complete the work-up.

MEDICAL DECISION MAKING

The first priority must always be supportive care in the management of the poisoned patient. Use all available historical

items to help identify the possible toxin. A thorough physical

exam including careful attention to the patient's mental

status, vital signs, pupillary size and responsiveness, the presence of seizures, or abnormal changes in skin color, tern ­

perature, and moisture may help classify the patient's

presentation into a specific toxidrome. Use the ancillary

studies described previously to help clarify the diagnosis and

guide further management (Figure 54-1).

TREATMENT

The treatment of poisoned patients can be broken down

into a very systematic approach outlined by the mnemonic

ABCDEFGH. First and foremost, initiate aggressive

supportive care. The airway and breathing must be secured

and addressed without delay. Intubation may be prevented

Toxic exposure or poisoning

Supportive care: Address ABC's, IV

ccess, supplemental 02- cardiac monitor

Lab studies, ECG, identify toxidromes,

contact poison control center

consider decontamination:

• Wash patient

• Activated charcoal

• Gastric lavage

• Whole bowel irrigation

Consider enhanced elimination:

• Mu lti-dose activated charcoal

• Urinary alkalinization

• Hemodialysis

Consider focused antidotal therapy

Figure 54-1 The poisoned patient

diag nostic algorithm. ABCs, airway,

breathing, and circu lation; ECG,

electrocard iogram; IV, intravenous.

with the successful use of a focused therapy such as

naloxone in opioid toxicity or supplemental dextrose in

hypoglycemic patients. Likewise, correct any circulatory

compromise in the form of hypotension or bradycardia

with standard fluid and/or vasopressor administration. Pay

careful attention to the core temperature. Aggressively and

expeditiously correct hyperpyrexia with active cooling measures and not systemic antipyretics. These measures, rather

than the early search for specific antidotes, are the cornerstone of the initial management of the poisoned patient.

The basic goal of decontamination is to remove the poison

from the patient and the patient from the poison. Attempt

decontamination as early as possible to achieve maximal

benefit. Washing a patient's skin with soap and water to

prevent further absorption and/or prevent harm to the

emergency staff (eg, a patient covered with an organophosphate) is the simplest form of decontamination. Activated

charcoal (1 g/kg or a 10:1 ratio of charcoal to toxin) can be

given orally to bind ingested poisons and limit further gastrointestinal (GI) absorption. Although most drugs are

THE POISONED PATIENT

amenable to this, lithium, iron and other metals, hydrocarbons, caustics, and toxic alcohols are not. Consider gastric

lavage in patients who present very early (within 1 hour)

after a potentially lethal ingestion. Additionally, any potentially fatal ingestions that don't have available antidotes may

warrant lavage regardless of the timing of ingestion (eg,

massive colchicine overdose). Contraindications to gastric

lavage include the ingestion of hydrocarbons or other caustic agents, and potential complications include increased

intracranial pressure, aspiration, and esophageal rupture.

Whole-bowel irrigation with polyethylene glycol

(GoLYTELY), given at a rate between 0.5 L/hr (pediatrics)

and 2 L/hr, may help to "flush" toxins that won't bind to

charcoal (eg, leaded paint chips) out of the GI tract and

therefore limit total absorption. Contraindications to

whole-bowel irrigation include hemodynamic instability

(hypotension = lack of GI perfusion) and decreased bowel

sounds (impaired GI motility). Of note, pulmonary aspira ­

tion is the most common adverse side effect for all forms of

GI decontamination, and patients must have an intact air ­

way for these procedures to be pursued.

There are several different modalities available to

enhance the elimination of poisons. Hemodialysis is ideal

for smaller-sized poisons with small volumes of distribution

( <1 L/kg) and low degrees of protein-binding. Ideal agents

for hemodialysis include aspirin, toxic alcohols, and lithium.

Hemodialysis should also be performed in all patients with

profound acidemia regardless of the etiology. Alkalinization

of the urine is commonly initiated for ingestions of weak

acids such as aspirin and phenobarbital. The proposed

mechanism depends on increasing the urinary pH by giving

doses of intravenous (IV) sodium bicarbonate. Circulating

toxins will be preferentially converted to their conjugate

bases in the alkaline environment and consequently trapped

in the renal tubules, where they will be excreted in the urine.

Alkalinization can also benefit patients in select cases ( eg,

salicylate overdose) by keeping the poison preferentially out

of the CNS, as the ionized form cannot enter through the

blood-brain barrier. Finally, multiple doses of oral activated

charcoal (MDAC) can be administered to patients poisoned

with select agents including theophylline, phenobarbital,

carbamazepine, dapsone, or quinine. The proposed mechanism relies on the use of the GI tract wall as a dialysis membrane. The intraluminal charcoal functions to pull

circulating toxins back into the GI tract where they are

bound to the charcoal and excreted. MDAC can also be

employed to further decontaminate the gut of agents that

have erratic and prolonged absorption ( eg, salicylates, val ­

proic acid). If MDAC is entertained, ensure that the charcoal is not premixed with sorbitol, as cathartics (unlike

polyethylene glycol) can cause marked fluid and electrolyte

shifts, resulting in significant morbidity and/or mortality.

Antidotal therapy is important and necessary when

managing the poisoned patient, but should never take

priority over the supportive measures already mentioned.

Examples of selected focused therapy along with general

indications are listed in Table 54-3. The final portion of the

Table 54-3. Specific antidotes for toxicologic agents.

Acetaminophen

Crotalidae bite

Poison

Hydrofluoric acid, calcium channel

antagonists

Cyanide

Iron

Digoxin

Ethylene glycol, methanol

Methanol, methotrexate

Calcium channel blocker, � blocker

Oxidizing chemicals (nitrites, benzocaine,

sulfonamides)

Refractory hypoglycemia after oral

hypoglycemic

Opioid, clonidine

Anticholinergic (not TCA)

Cholinergic

Heparin

Isoniazid

Anticoagulants

TCA, tricyclic antidepressant.

Antidote

N-acetylcysteine

Antivenom Fab

Calcium gluconate or

calcium chloride

Sodium nitrite, thiosulfate

Deferoxamine

Digoxin Fab

Fomepizole or ethanol

Folic acid/leucovorin

Glucagon

Methylene blue

Octreotide

Naloxone

Physostigmine

Pralidoxime (HAM)

Protamine

Pyridoxine

Vitamin K

management algorithm includes G and H. This is a

reminder for clinicians to never hesitate in calling their

regional poison center ( 1-800-222-1222) for assistance

during any point in the care of the poisoned patient.

Getting help early may facilitate a more focused work-up,

prevent unnecessary laboratory and/or diagnostic studies,

provide insight into potentially life-saving antidotal

therapy, and assist with appropriate disposition making.