, temporarily take patient off 0

2 and repeat evaluation)

History of loss of consciousness or near-syncope

History of seizure

Coma

History of hypotension during or shortly after exposure

Myocardial ischemia

History of prolonged exposure

Pregnancy with COHb >15%

DISPOSITION

...,._ Admission

Patients with any signs of hemodynamic instability warrant

admission to a critical care setting. Furthermore, admit all

patients with altered mental status or other neurologic deficits and those with indications for HBO to a critical care or

monitored setting. Well-appearing patients with no signs of

active toxicity whose poisoning was due to a suicide attempt

require psychiatric evaluation and admission.

...,._ Discharge

Patients with accidental exposures who are clinically well

with COHb levels <5% after 100% 02 treatment can be

safely discharged. Educate all discharged patients about

CO poisoning and encourage them to have their homes

examined by the fire department or gas company. Convey

the importance of a home CO detector. Provide adequate

Relative Indication

Persisting neurologic symptoms including headache and dizziness after

4 hours of 1 00% normobaric 0

2

Persisting acidosis

Concurrent thermal or chemical burns

Pregnancy with history of carbon monoxide exposure regardless of

COHb level

follow-up to assess for the development of delayed

neurological sequelae .

SUGGESTED READING

Maloney G. Carbon monoxide. In: Tintinalli JE, Kelen GD,

Stapczynski JS, eds. Tintinalli's Emergency Medicine: A

Comprehensive Study Guide. 7th ed. New York, NY: McGrawHill, 201 1.

Nelson LS, Lewin NA, Howland MA, Hoffman RS, Goldfrank

LR, Flomenbaum NE. Goldfrank's Toxicologic Emergencies.

9th ed. New York, NY: McGraw-Hill, 20 11.

Weaver LK. Carbon monoxide poisoning. N Engl J Med.

2009;360: 1217.

Wolf SJ, Lavonas EJ, Sloan EP, J agoda AS, American College of

Emergency Physicians. Critical issues in the management of

adult patients presenting to the emergency department with

acute carbon monoxide poisoning. Ann Emerg Med.

2008;5 1: 138-152.

Digoxin

Michael E. Nelson, MD

Key Points

• Attempt to disti nguish between acute versus chronic

ingestions, as the symptoms and treatments differ.

• Electrocardiogram changes are common and include

downward-sloping (scooped) ST-segment depressions,

premature ventricular complexes, supraventricu lar

dysrhythmias with slow ventricular rates, and

bidirectional ventricular tachycardia.

INTRODUCTION

Digoxin, a commonly prescribed agent derived from the

foxglove plant, belongs to a class of medications known as

cardiac glycosides. These agents function to increase myocardial contractility and slow AV nodal conduction and are

commonly used for the treatment of congestive heart failure

and various cardiac dysrhythmias including atrial fibrillation. Of interest, cardiac glycosides are frequently encountered in the natural world as a predatory deterrent in both

plant and animal species, including oleander, lily of the

valley, red squill, and bufo toads. The relative potency of

digoxin lends to a very narrow therapeutic window, and lifethreatening toxicity can develop with both acute overdoses

and chronic excessive exposures. Poisoned patients generally

present with variable symptoms and must be viewed in light

of acute versus chronic versus acute on chronic exposures. If

left untreated, death will invariably result secondary to cardiac instability and hemodynanlic compromise.

As a whole, cardiac glycosides were responsible for

nearly 2,500 poisonings reported to the National Poison

Data System in the year 2010. They were the third most

common cardiovascular agent implicated in patient toxicity and were the primary agent responsible for 17 patient

deaths. Of note, clinically significant toxicity is far more

251

• Although hyperkalemia can be a marker of significant

digoxin poisoning, standard treatment with intravenous

calcium should typically be avoided.

• Empirically administer digoxin-specific antibodies (5 vials for chronic toxicity, 1 0-20 vials for acute ingestions)

to all patients with life-threatening dysrhythmias or

hemodynamic instabil ity.

common in pediatric and geriatric populations. Pediatric

overdoses arise from iatrogenic dosing errors or accidental

ingestions of adult medications, whereas geriatric t oxicity

generally results from either drug-drug interactions or

alterations in metabolic clearance. Intentional overdoses

are most common in adult patients and can be of both the

acute and chronic variety.

Orally administered digoxin begins to exhibit clinical

effects within 90 minutes of ingestion and typically reaches

maximal effect within 4-6 hours. Digoxin is primarily

eliminated by the kidneys with a usual half-life of

36-48 hours.