mia in the standard fashion with sodium bicarbonate,

albuterol nebulizers, glucose with insulin, and sodium

polystyrene sulfonate (Kayexalate), but avoid empiric

treatment with intravenous (IV) calcium due to the

theoretical risk of "stone heart" and fatal dysrhythmias.

That said, N calcium can be given to patients with severe

Check serum

digoxin level and

electrolytes

Consider digibind therapy if:

1) Hyperkalemia

2} Elevated digoxin level

3} Borderline BP or HR

Figure 59-2. Digoxin diag nostic algorithm. BP, blood pressure; ECG,

electroca rd iogram; H R, heart rate.

CHAPTER 59

hyperkalemic cardiotoxicity (sinus arrest, sinusoidal

rhythm) refractive to alternative treatments. In patients

with chronic toxicity, carefully supplement serum hypokalemia and hypomagnesemia to prevent overcorrection.

Treat significant bradycardias and/or AV nodal conduction

disturbances with IV atropine (0.5-2 mg).

Digoxin-specific antibodies (Digibind, Digoxin Fab

fragments) provide an eloquent and effective method for

treating digoxin toxicity. Indications for use include significant dysrhythmias, hypotension, and hyperkalemia secondary to cardiac glycoside ingestion. Although no absolute

contraindications exist, exercise caution in patients with a

known hypersensitivity to ovine (sheep) derived products.

The appropriate dose of Fab fragments can be determined

by 1 of 3 ways and is based on the total body burden of

digoxin. After an acute ingestion, digoxin has a roughly

80% bioavailability and each vial of Fab fragments can bind

0.5 mg of circulating digoxin. Based on this, the proper dose

of Fab fragments can be calculated as follows:

1. Known quantity of ingested digoxin:

Number of Fab vials = [ (Amount of digoxin ingested (mg)

X 0.8)/0.5]

Rounded-up to the nearest whole number

2. Measured serum digoxin concentrations:

Number of Fab vials = [Serum digoxin level (ng!mL)

X patient weight (kg) ] /100

Rounded-up to the nearest whole number

3. Patients demonstrating significant toxicity (lifethreatening dysrhythmias, profound hypotension, and/

or severe hyperkalemia):

Empirically treat acute ingestions with 10-20 vials of

Fab fragments and chronic exposures with 5 vials.

Repeated dosing may be required.

Of note, most lab assays do not distinguish between free

and bound digoxin, and serum levels lose their c linical utility after the administration of Fab fragments. Furthermore,

treatment with Fab fragments may lead to the secondary

decompensation of underlying cardiac conditions such as

CHF or atrial fibrillation, which had been previously controlled with digoxin therapy.

DISPOSITION

� Admission

Admit all patients after a potentially significant ingestion

who either have a history of significant comorbid

conditions or exhibit signs or symptoms of clinical toxicity

including cardiovascular instability, dysrhythmias, GI

distress, and mental status changes. Any patient with

toxicity significant enough to warrant digoxin Fab

fragments requires admission to an intensive care unit

setting. Patients who ingest digoxin as part of a suicide

attempt warrant psychiatric evaluation once they are

medically stabile.

� Discharge

Patients with accidental ingestions and no significant

comorbidities who remain symptom free after an 8- to

12-hour observation period may be safely discharged home.

SUGGESTED READING

Boyle JS, Kirk MA. Digitalis glycosides. In: Tintinalli JE,

Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD.

Tintinalli's Emergency Medicine: A Comprehensive Study Guide.

7th ed. New York, NY: McGraw-Hill, 201 1, pp. 1260-1264.

Hack JB. Cardioactive steroids. In: Nelson LS, Lewin NA,

Howland MA, et al. Go/drank's Toxicologic Emergencies. 9th ed.

New York, NY: McGraw-Hill, 20 1 1, pp. 936-945.

Ma G, Brady WJ, Pollack M, Chan TC. Electrocardiographic

manifestations: digitalis toxicity. ] Emerg Med. 200 1;20: 145-152.

Manini AF, Nelson LS, Hoffman RS. Prognostic utility of serum

potassium in chronic digoxin toxicity. Am J Cardiovasc Drugs.

20 1 1; 1 1:173-178.

Cyclic Antidepressants

Harry C. Karydes, DO

Key Points

• Cyclic antidepressants remain a leading cause of

poisoning-related fatalities among psychoactive

medications.

• Patients will frequently present with minimal signs

and symptoms only to abruptly decompensate from

l ife-threatening card iovascular and central nervous

system toxicity.

INTRODUCTION

Cyclic antidepressants (CA) consist of a group of pharmacologically related medications that were initially developed

in the late 1950s for the treatment of patients with severe

depression. Although used less frequently for this purpose,

their role has expanded to include the management of

various alternative conditions including neuralgic pain,

migraine headaches, enuresis, and attention deficit hyperactivity disorder. Traditional cyclic antidepressants have a

chemical structure built on a 3-ring nucleus and include

such medications such as amitriptyline, nortriptyline, doxepin, imipramine, and clomipramine. Antidepressants have

historically remained a leading cause of pharmacologic

self-poisoning owing to their near ubiquitous availability to

a depressed patient population inherently at risk for selfharming behavior. Although the introduction of selective

serotonin reuptake inhibitors (SSRls) has decreased the

overall incidence of CA poisonings, CA overdoses c ontinue

to account for a greater morbidity and mortality given their

increased potential for significant toxicologic complications, especially in pediatric patients.

Cyclic antidepressants are nonselective agents that

exhibit a wide array of pharmacologic effects with consid ­